Distribution of macrophage polarization markers in human atherosclerosis
Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis. We used transcriptomics and immunohistochemistry to analyze macrophage...
Saved in:
| Published in: | Atherosclerosis Vol. 225; no. 2; pp. 461 - 468 |
|---|---|
| Main Authors: | , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Amsterdam
Elsevier Ireland Ltd
01.12.2012
Elsevier |
| Subjects: | |
| ISSN: | 0021-9150, 1879-1484, 1879-1484 |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Abstract | Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis.
We used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68+ areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers.
M1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis.
► We assessed macrophage subsets in human plaques through transcriptomics and IHC. ► Signatures for M1 and M2 macrophage subsets persist throughout plaque progression. ► M1 and M2 macrophages display different distribution patterns in the vessel wall. ► M1 macrophages dominate plaque shoulders, a predilection site for rupture. ► Macrophage polarization state could hold substantial influence over plaque outcome. |
|---|---|
| AbstractList | Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis.OBJECTIVEMacrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis.We used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68(+) areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers.METHODS & RESULTSWe used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68(+) areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers.M1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis.CONCLUSIONM1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis. Abstract Objective Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis. Methods & results We used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68+ areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers. Conclusion M1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis. Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis. We used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68(+) areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers. M1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis. Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis. We used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68+ areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers. M1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis. ► We assessed macrophage subsets in human plaques through transcriptomics and IHC. ► Signatures for M1 and M2 macrophage subsets persist throughout plaque progression. ► M1 and M2 macrophages display different distribution patterns in the vessel wall. ► M1 macrophages dominate plaque shoulders, a predilection site for rupture. ► Macrophage polarization state could hold substantial influence over plaque outcome. OBJECTIVE: Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial distribution of polarized macrophage populations in human atherosclerosis. METHODS & RESULTS: We used transcriptomics and immunohistochemistry to analyze macrophage subset dynamics in successive stages of atherogenesis. Developing lesions progressively accumulated both M1 and M2 cells, as was signified by the enhanced expression of associated markers at the transcriptional and protein level. Histologically, these markers were confined to overlapping, but spatially distinct CD68⁺ areas of the intima. We subsequently quantified the presence of these markers in relation to morphological determinants of plaque stability. In line with their pro-inflammatory characteristics, M1 macrophages dominated the rupture-prone shoulder regions of the plaque over M2 polarized cells, while the fibrous caps of lesions showed no significant differences between subsets. In contrast, vascular adventitial tissue displayed a pronounced M2 activation profile. As expected, areas of intraplaque hemorrhage clearly associated with CD163 staining. Rather than being limited to complicated lesions, this M2 marker was also readily detectable in stable plaques. Finally, foamy macrophages displayed an ambiguous repertoire that incorporates individual M1 and M2 markers. CONCLUSION: M1 and M2 macrophage populations are present throughout atherogenesis. These subsets display disparity when it comes to their prevalence in morphological compartments of the vessel wall. Our current findings warrant continued investigation into the functional implications of polarized macrophage populations in human atherosclerosis. |
| Author | Daemen, Mat J.A.P. Gijbels, Marion J.J. Stöger, J. Lauran Lutgens, Esther van der Velden, Saskia van der Loos, Chris M. Manca, Marco de Winther, Menno P.J. Biessen, Erik A.L. |
| Author_xml | – sequence: 1 givenname: J. Lauran surname: Stöger fullname: Stöger, J. Lauran organization: Dept. of Molecular Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, 6229ER Maastricht, The Netherlands – sequence: 2 givenname: Marion J.J. surname: Gijbels fullname: Gijbels, Marion J.J. organization: Dept. of Molecular Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, 6229ER Maastricht, The Netherlands – sequence: 3 givenname: Saskia surname: van der Velden fullname: van der Velden, Saskia organization: Dept. of Medical Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands – sequence: 4 givenname: Marco surname: Manca fullname: Manca, Marco organization: Dept. of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands – sequence: 5 givenname: Chris M. surname: van der Loos fullname: van der Loos, Chris M. organization: Dept. of Pathology, Academic Medical Center, Amsterdam, The Netherlands – sequence: 6 givenname: Erik A.L. surname: Biessen fullname: Biessen, Erik A.L. organization: Dept. of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands – sequence: 7 givenname: Mat J.A.P. surname: Daemen fullname: Daemen, Mat J.A.P. organization: Dept. of Pathology, Academic Medical Center, Amsterdam, The Netherlands – sequence: 8 givenname: Esther surname: Lutgens fullname: Lutgens, Esther organization: Dept. of Medical Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands – sequence: 9 givenname: Menno P.J. surname: de Winther fullname: de Winther, Menno P.J. email: m.dewinther@amc.uva.nl organization: Dept. of Medical Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26619613$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/23078881$$D View this record in MEDLINE/PubMed |
| BookMark | eNqVkk1v1DAQhi1URD_gL0AulbjsMnYcfxxAqpbSIlXiUHq2HGfS9TYbL3aCVH49zu4C0kqIcrEPfub1zPvOKTnqQ4-EnFOYU6Di3WpuhyXGkFw3nT7NGVA2Bz0HWj4jJ1RJPaNc8SNyAsDoTNMKjslpSisA4JKqF-SYlSCVUvSEXH_0aYi-Hgcf-iK0xdq6GDZLe4_FJnQ2-h92-7S28QFjKnxfLMe17YuDNl6S563tEr7a32fk7tPl18X17ObL1efFxc3MSS6HGa90q5XljoMVsgZUVJRUON0IzUrFsamauhWshpLJhrNaQ22ZyCDKBllTnpG3O91NDN9GTINZ--Sw62yPYUyGCslA6bKS_0ap1BVXVIuMvt6jY73GxmyizwM_ml9GZeB8D9jkbNdG2zuf_nBCZBlaZu79jssuphSx_Y1QMFOAZmUOnDNTgAa0gW394qDe-WGbwBCt756s8man0tpg7H3Mz3e3GaimFcjz8Exc7QjMWX33GE1yHnuHjY_oBtME_-S_Phwouc73Ppv0gI-YVmGMfV4IQ03KNeZ2WsppJykDyNFPrVz-XeA_GvkJrwH6zw |
| CitedBy_id | crossref_primary_10_1016_j_ejpb_2019_12_005 crossref_primary_10_1016_j_febslet_2015_01_002 crossref_primary_10_3389_fcvm_2022_894879 crossref_primary_10_3389_fimmu_2014_00612 crossref_primary_10_1160_TH16_04_0318 crossref_primary_10_1155_2019_4354786 crossref_primary_10_3389_fcvm_2022_948461 crossref_primary_10_1016_j_molmed_2021_09_004 crossref_primary_10_1007_s13577_021_00580_6 crossref_primary_10_1111_sji_12314 crossref_primary_10_1016_j_bone_2020_115560 crossref_primary_10_1155_2019_7434376 crossref_primary_10_1038_s41467_020_18287_x crossref_primary_10_1160_TH16_08_0593 crossref_primary_10_3109_1040841X_2014_932327 crossref_primary_10_1007_s13205_024_03924_9 crossref_primary_10_1177_00033197211012539 crossref_primary_10_1155_2013_198193 crossref_primary_10_1186_s11658_022_00384_y crossref_primary_10_1186_s12933_022_01497_6 crossref_primary_10_3389_fphys_2022_848867 crossref_primary_10_1038_s41467_021_26777_9 crossref_primary_10_3390_ijms23094808 crossref_primary_10_1002_adhm_202302835 crossref_primary_10_1016_j_phrs_2020_104664 crossref_primary_10_1002_adhm_202000336 crossref_primary_10_3390_biomedicines11123275 crossref_primary_10_1093_infdis_jix082 crossref_primary_10_1093_infdis_jix085 crossref_primary_10_1016_j_freeradbiomed_2015_08_010 crossref_primary_10_1016_j_biopha_2022_114201 crossref_primary_10_3389_fimmu_2014_00510 crossref_primary_10_1016_j_surg_2017_10_051 crossref_primary_10_1146_annurev_bioeng_062117_121224 crossref_primary_10_1080_08830185_2025_2489346 crossref_primary_10_1016_j_jep_2023_117070 crossref_primary_10_1093_cvr_cvab301 crossref_primary_10_1161_CIRCULATIONAHA_121_054285 crossref_primary_10_1186_s13550_019_0474_0 crossref_primary_10_1038_nutd_2017_15 crossref_primary_10_1186_s40169_014_0042_1 crossref_primary_10_14412_1995_4484_2018_486_493 crossref_primary_10_1096_fj_202201486R crossref_primary_10_1111_bph_13705 crossref_primary_10_1007_s10753_019_01146_3 crossref_primary_10_1097_MOL_0b013e32836484a4 crossref_primary_10_3892_mmr_2020_11023 crossref_primary_10_1016_j_atherosclerosis_2020_07_017 crossref_primary_10_1186_s12967_017_1187_7 crossref_primary_10_1016_j_cca_2019_10_034 crossref_primary_10_1007_s00011_014_0762_0 crossref_primary_10_1016_j_gene_2021_145534 crossref_primary_10_1016_j_nucmedbio_2021_09_003 crossref_primary_10_1038_s41536_021_00193_5 crossref_primary_10_1039_c6ib00105j crossref_primary_10_1111_cpr_70012 crossref_primary_10_1007_s00395_023_01027_9 crossref_primary_10_1016_j_atherosclerosis_2014_10_106 crossref_primary_10_1161_ATVBAHA_115_305630 crossref_primary_10_1038_s41467_020_20141_z crossref_primary_10_3389_fcvm_2022_868788 crossref_primary_10_1016_j_bbrc_2019_02_005 crossref_primary_10_3389_ebm_2025_10624 crossref_primary_10_1109_TNANO_2017_2771311 crossref_primary_10_3109_08916934_2015_1027815 crossref_primary_10_3389_fimmu_2014_00537 crossref_primary_10_1007_s00424_017_1942_x crossref_primary_10_3389_fimmu_2025_1607932 crossref_primary_10_1016_j_biopha_2017_11_061 crossref_primary_10_1016_j_heliyon_2024_e32073 crossref_primary_10_1124_jpet_122_001284 crossref_primary_10_1016_j_immuni_2017_09_008 crossref_primary_10_1038_s41598_024_68333_7 crossref_primary_10_1136_bjsports_2018_099677 crossref_primary_10_1160_TH15_08_0650 crossref_primary_10_1016_j_jff_2016_08_037 crossref_primary_10_1371_journal_pone_0151057 crossref_primary_10_3389_fimmu_2023_1295257 crossref_primary_10_1016_j_jss_2019_06_060 crossref_primary_10_1016_j_atherosclerosis_2016_05_021 crossref_primary_10_1016_j_matbio_2018_05_007 crossref_primary_10_1016_j_tem_2013_10_007 crossref_primary_10_1161_ATVBAHA_122_317898 crossref_primary_10_4049_jimmunol_1800065 crossref_primary_10_1155_2014_276457 crossref_primary_10_1161_CIRCRESAHA_116_309492 crossref_primary_10_1016_j_biopha_2020_110915 crossref_primary_10_1186_s12931_017_0522_0 crossref_primary_10_1002_JLB_4RI0518_183R crossref_primary_10_1016_j_atherosclerosis_2021_08_010 crossref_primary_10_1093_ndt_gfw214 crossref_primary_10_4049_jimmunol_1402797 crossref_primary_10_1080_14779072_2022_2111301 crossref_primary_10_1160_TH14_06_0509 crossref_primary_10_1159_000501558 crossref_primary_10_1093_jleuko_qiaf060 crossref_primary_10_1007_s00395_024_01033_5 crossref_primary_10_3390_ijms26031019 crossref_primary_10_1177_1358863X19878495 crossref_primary_10_1113_EP085569 crossref_primary_10_1016_j_atherosclerosis_2015_02_005 crossref_primary_10_1016_j_cjca_2016_12_010 crossref_primary_10_1089_dna_2018_4552 crossref_primary_10_1016_j_bone_2021_115942 crossref_primary_10_3390_antiox11081529 crossref_primary_10_1371_journal_pone_0130484 crossref_primary_10_1093_ehjci_jeae314 crossref_primary_10_2174_1381612827666210118121952 crossref_primary_10_1016_j_ejphar_2017_10_005 crossref_primary_10_1016_j_atherosclerosis_2020_06_010 crossref_primary_10_1038_srep35234 crossref_primary_10_3892_etm_2018_5711 crossref_primary_10_1063_5_0168087 crossref_primary_10_1038_s41569_021_00629_x crossref_primary_10_1371_journal_pone_0128163 crossref_primary_10_3390_ijms25020951 crossref_primary_10_1002_1873_3468_12029 crossref_primary_10_1007_s11307_017_1117_3 crossref_primary_10_3389_fendo_2018_00002 crossref_primary_10_1007_s00109_023_02359_8 crossref_primary_10_1186_s40729_021_00391_2 crossref_primary_10_1161_ATVBAHA_116_307573 crossref_primary_10_1016_j_intimp_2019_02_054 crossref_primary_10_3389_fimmu_2014_00579 crossref_primary_10_3390_antiox11122356 crossref_primary_10_1038_s41598_020_71110_x crossref_primary_10_1186_s12967_021_02727_3 crossref_primary_10_1042_CS20220531 crossref_primary_10_3389_fimmu_2017_00289 crossref_primary_10_1016_j_atherosclerosis_2015_09_010 crossref_primary_10_1177_0300060518787671 crossref_primary_10_1016_j_coph_2013_01_003 crossref_primary_10_1007_s12013_014_9987_3 crossref_primary_10_1080_14728222_2022_2037556 crossref_primary_10_1111_jocd_15098 crossref_primary_10_1039_D1RA08061J crossref_primary_10_1016_j_atherosclerosis_2017_02_021 crossref_primary_10_1093_eurheartj_ehaf289 crossref_primary_10_1007_s00011_021_01498_3 crossref_primary_10_1111_imr_12218 crossref_primary_10_1084_jem_20150900 crossref_primary_10_1016_j_jconrel_2021_04_018 crossref_primary_10_4049_jimmunol_1300990 crossref_primary_10_1007_s00395_023_01023_z crossref_primary_10_1155_2016_9582430 crossref_primary_10_3390_ijms25179737 crossref_primary_10_4049_jimmunol_1601445 crossref_primary_10_1016_j_freeradbiomed_2022_02_010 crossref_primary_10_1177_2047487317743355 crossref_primary_10_3390_ijms232112906 crossref_primary_10_1111_cpr_13175 crossref_primary_10_1161_ATVBAHA_113_303153 crossref_primary_10_3390_cryst11070735 crossref_primary_10_3389_fcvm_2022_1046273 crossref_primary_10_1016_j_carpath_2020_107258 crossref_primary_10_1097_CM9_0000000000000333 crossref_primary_10_3390_ijms23094513 crossref_primary_10_1161_HCG_0000000000000037 crossref_primary_10_1016_j_tcm_2018_09_017 crossref_primary_10_1093_cvr_cvv227 crossref_primary_10_1186_s13062_025_00621_2 crossref_primary_10_3389_fphar_2019_00536 crossref_primary_10_3390_biomedicines10020452 crossref_primary_10_1111_jcmm_13329 crossref_primary_10_33549_physiolres_932858 crossref_primary_10_1161_ATVBAHA_114_303866 crossref_primary_10_3389_fimmu_2019_01330 crossref_primary_10_1080_10641963_2017_1288740 crossref_primary_10_3389_fimmu_2023_1185587 crossref_primary_10_3390_nu7085324 crossref_primary_10_1371_journal_pone_0195657 crossref_primary_10_1016_j_atherosclerosis_2016_03_012 crossref_primary_10_1155_2017_4080364 crossref_primary_10_1016_j_rvsc_2022_02_006 crossref_primary_10_1186_s13075_022_02938_z crossref_primary_10_1084_jem_20190459 crossref_primary_10_1186_s12967_020_02226_x crossref_primary_10_3389_fimmu_2016_00275 crossref_primary_10_3389_fphar_2019_00666 crossref_primary_10_1080_08830185_2020_1768251 crossref_primary_10_1016_j_cpcardiol_2022_101311 crossref_primary_10_1161_ATVBAHA_125_323005 crossref_primary_10_1371_journal_ppat_1008869 crossref_primary_10_1111_jre_12773 crossref_primary_10_1038_s41419_019_2109_9 crossref_primary_10_1371_journal_pone_0183572 crossref_primary_10_3390_ijms23010077 crossref_primary_10_3389_fimmu_2022_1045624 crossref_primary_10_1016_j_arcmed_2013_11_007 crossref_primary_10_1016_j_atherosclerosis_2025_119180 crossref_primary_10_3389_fimmu_2020_00397 crossref_primary_10_1007_s10557_014_6556_3 crossref_primary_10_1016_j_hermed_2022_100558 crossref_primary_10_3390_cells12151936 crossref_primary_10_3389_fimmu_2024_1437821 crossref_primary_10_1038_s41419_023_06206_z crossref_primary_10_1016_j_maturitas_2017_07_014 crossref_primary_10_3389_fphys_2020_599379 crossref_primary_10_3389_fphar_2022_898067 crossref_primary_10_1016_j_yexcr_2020_112194 crossref_primary_10_1155_2021_6957900 crossref_primary_10_1007_s10753_015_0263_5 crossref_primary_10_1096_fj_13_235911 crossref_primary_10_1136_bcr_2021_248539 crossref_primary_10_3389_fonc_2023_1103149 crossref_primary_10_1186_s12944_017_0647_7 crossref_primary_10_1016_j_intimp_2017_11_037 crossref_primary_10_1016_j_atherosclerosis_2017_10_009 crossref_primary_10_1007_s00395_016_0554_5 crossref_primary_10_1016_j_tox_2020_152404 crossref_primary_10_1016_j_smim_2015_03_013 crossref_primary_10_1016_j_vph_2018_08_003 crossref_primary_10_3389_fcvm_2023_1264901 crossref_primary_10_1016_j_vph_2018_08_002 crossref_primary_10_3389_fcvm_2024_1450737 crossref_primary_10_1111_clr_14448 crossref_primary_10_3389_fimmu_2023_1152881 crossref_primary_10_3389_fimmu_2023_1195699 crossref_primary_10_4103_JHCR_JHCR_10_23 crossref_primary_10_1111_jcmm_70220 crossref_primary_10_1111_joim_12367 crossref_primary_10_1161_ATVBAHA_118_307742 crossref_primary_10_1016_j_bbadis_2016_03_004 crossref_primary_10_1177_17534259221090679 crossref_primary_10_4049_jimmunol_1800002 crossref_primary_10_1111_acel_12416 crossref_primary_10_1111_jpi_12581 crossref_primary_10_3389_fphar_2022_906512 crossref_primary_10_3390_biomedicines13081802 crossref_primary_10_1007_s00395_022_00972_1 crossref_primary_10_1111_1755_5922_12262 crossref_primary_10_1016_j_trsl_2017_10_004 crossref_primary_10_1002_biof_1243 crossref_primary_10_1016_j_intimp_2023_109877 crossref_primary_10_1155_2021_5217572 crossref_primary_10_1186_s13287_021_02490_8 crossref_primary_10_1186_s12933_024_02339_3 crossref_primary_10_3892_mmr_2024_13269 crossref_primary_10_1016_j_atherosclerosis_2020_03_008 crossref_primary_10_1093_toxsci_kfad001 crossref_primary_10_1016_j_jnutbio_2015_11_002 crossref_primary_10_1126_sciimmunol_aah4081 crossref_primary_10_3390_ijms20215293 crossref_primary_10_1097_IN9_0000000000000032 crossref_primary_10_1016_j_arabjc_2023_104796 crossref_primary_10_1093_cvr_cvw016 crossref_primary_10_1186_s13018_022_03029_0 crossref_primary_10_15252_emmm_201404170 crossref_primary_10_1016_j_lfs_2024_123204 crossref_primary_10_3109_1354750X_2014_915342 crossref_primary_10_3389_fmolb_2021_679797 crossref_primary_10_1097_MOL_0000000000000217 crossref_primary_10_1177_1074248415575967 crossref_primary_10_1016_j_freeradbiomed_2018_09_001 crossref_primary_10_3389_fphar_2023_1252907 crossref_primary_10_1161_ATVBAHA_119_312802 crossref_primary_10_1016_j_fct_2021_112111 crossref_primary_10_1161_CIRCRESAHA_114_302721 crossref_primary_10_1097_MOL_0000000000000447 crossref_primary_10_1007_s12350_014_9959_4 crossref_primary_10_1039_D2BM00125J crossref_primary_10_1002_cam4_2327 crossref_primary_10_1080_07853890_2025_2453826 crossref_primary_10_1186_s12872_021_02420_9 crossref_primary_10_1007_s00784_020_03556_2 crossref_primary_10_1016_j_bioactmat_2021_04_017 crossref_primary_10_1016_j_chemphyslip_2023_105362 crossref_primary_10_1016_j_coi_2020_09_005 crossref_primary_10_1016_j_imbio_2013_06_005 crossref_primary_10_1016_j_clim_2019_03_001 crossref_primary_10_1161_ATVBAHA_124_322067 crossref_primary_10_1016_j_psj_2024_104558 crossref_primary_10_1172_JCI154217 crossref_primary_10_1016_j_ijbiomac_2025_145824 crossref_primary_10_1371_journal_pone_0078045 crossref_primary_10_1177_17534259251326700 crossref_primary_10_2147_DDDT_S487476 crossref_primary_10_1002_eji_202350464 crossref_primary_10_1155_2015_851252 crossref_primary_10_1371_journal_pone_0160449 crossref_primary_10_3389_fphys_2023_1179828 crossref_primary_10_1016_j_biopha_2020_110015 crossref_primary_10_1002_cph4_70008 crossref_primary_10_3892_etm_2024_12453 crossref_primary_10_1155_2016_9153673 crossref_primary_10_3390_ijms251910381 crossref_primary_10_1016_j_neurobiolaging_2016_08_004 crossref_primary_10_3390_ijms251810146 crossref_primary_10_1111_imm_12126 crossref_primary_10_1186_s13045_018_0637_x crossref_primary_10_1155_2020_8881683 crossref_primary_10_1007_s43939_024_00133_2 crossref_primary_10_3390_ijms19061801 crossref_primary_10_36290_kar_2017_023 crossref_primary_10_1016_j_immuni_2013_06_009 crossref_primary_10_1161_ATVBAHA_112_300171 crossref_primary_10_2147_DDDT_S368836 crossref_primary_10_1161_ATVBAHA_112_300173 crossref_primary_10_1016_j_atherosclerosis_2015_08_029 crossref_primary_10_1186_s13075_017_1310_4 crossref_primary_10_1016_j_ijcard_2015_03_055 crossref_primary_10_1161_CIRCRESAHA_120_316770 crossref_primary_10_3389_fphar_2024_1378787 crossref_primary_10_1016_j_thromres_2017_04_024 crossref_primary_10_1016_j_vph_2017_10_005 crossref_primary_10_3389_fimmu_2022_910444 crossref_primary_10_1053_j_gastro_2014_02_007 crossref_primary_10_3389_fcvm_2022_954283 crossref_primary_10_3389_fimmu_2024_1330461 crossref_primary_10_1093_cvr_cvt097 crossref_primary_10_1016_j_jep_2023_116742 crossref_primary_10_1007_s00125_017_4330_3 crossref_primary_10_1007_s10741_018_09764_z crossref_primary_10_1016_j_ajpath_2025_05_014 crossref_primary_10_3390_ijms22136995 crossref_primary_10_1161_STROKEAHA_120_032964 crossref_primary_10_1186_s12866_019_1403_0 crossref_primary_10_3389_fimmu_2023_1200259 crossref_primary_10_1038_nrcardio_2014_173 crossref_primary_10_1159_000348795 crossref_primary_10_1177_1479164115582351 crossref_primary_10_1016_j_bcp_2022_115357 crossref_primary_10_1172_JCI82719 crossref_primary_10_1515_chem_2019_0125 crossref_primary_10_1096_fba_2025_00037 crossref_primary_10_3389_fcell_2021_724699 crossref_primary_10_3390_cells10010015 crossref_primary_10_3389_fimmu_2020_594136 crossref_primary_10_3389_fcell_2024_1446758 crossref_primary_10_3390_vetsci9030105 crossref_primary_10_1002_anbr_202100133 crossref_primary_10_1371_journal_pone_0152922 crossref_primary_10_1038_s41569_019_0265_3 crossref_primary_10_1016_j_biomaterials_2019_119378 crossref_primary_10_1371_journal_pone_0188530 crossref_primary_10_1161_JAHA_122_026174 crossref_primary_10_1186_ar4609 crossref_primary_10_2174_0109298673303369240312092913 crossref_primary_10_3390_ijms232214154 crossref_primary_10_1016_j_atherosclerosis_2015_04_798 crossref_primary_10_1016_j_jmbbm_2025_107139 crossref_primary_10_1007_s11883_024_01229_z crossref_primary_10_1097_XCE_0000000000000172 crossref_primary_10_1016_j_ajpath_2017_05_014 crossref_primary_10_1038_modpathol_2016_78 crossref_primary_10_2478_jtim_2022_0012 crossref_primary_10_1016_j_bbalip_2016_02_006 crossref_primary_10_1161_JAHA_115_002860 crossref_primary_10_3390_cancers16162801 crossref_primary_10_1016_j_ijcard_2018_01_008 crossref_primary_10_1161_ATVBAHA_114_304292 crossref_primary_10_3390_biomedicines12122683 crossref_primary_10_3390_ijms25084351 crossref_primary_10_1038_srep17135 crossref_primary_10_3389_fbioe_2025_1640560 crossref_primary_10_3390_biology12070896 crossref_primary_10_1007_s12265_024_10579_7 crossref_primary_10_1038_s41563_018_0190_6 crossref_primary_10_1016_j_atherosclerosis_2020_05_003 crossref_primary_10_1016_j_intimp_2020_106473 crossref_primary_10_1007_s12265_016_9678_0 crossref_primary_10_1007_s00018_015_1971_6 crossref_primary_10_4239_wjd_v14_i10_1478 crossref_primary_10_1186_s12967_015_0687_6 crossref_primary_10_1371_journal_pone_0156364 crossref_primary_10_18087_cardio_2019_1_10207 crossref_primary_10_1186_s12964_024_01473_5 crossref_primary_10_1016_j_omtn_2021_10_027 crossref_primary_10_1016_j_jjcc_2021_10_015 crossref_primary_10_3390_ijms24032600 crossref_primary_10_5812_jjnpp_62317 crossref_primary_10_1038_onc_2017_1 crossref_primary_10_1113_EP087827 crossref_primary_10_1016_j_gtc_2020_04_009 crossref_primary_10_1016_j_vph_2016_08_004 crossref_primary_10_3389_fcvm_2018_00032 crossref_primary_10_1155_2022_7421265 crossref_primary_10_1111_nyas_13009 crossref_primary_10_3389_fonc_2023_1213347 crossref_primary_10_3390_biomedicines9010084 crossref_primary_10_2147_JIR_S276982 crossref_primary_10_1093_cvr_cvz162 crossref_primary_10_3390_ijms24032613 crossref_primary_10_2147_IJN_S430877 crossref_primary_10_1161_ATVBAHA_117_309383 crossref_primary_10_1002_adtp_202100232 crossref_primary_10_1016_j_jpha_2023_11_016 crossref_primary_10_3390_ijms22179119 crossref_primary_10_1016_j_coph_2016_02_006 crossref_primary_10_1111_bjd_14471 crossref_primary_10_1093_rb_rbac064 crossref_primary_10_1016_j_lfs_2020_117837 crossref_primary_10_1016_j_intimp_2023_110546 crossref_primary_10_3389_fphar_2022_1034870 crossref_primary_10_1016_j_intimp_2022_109392 crossref_primary_10_1063_5_0087699 crossref_primary_10_1177_1358863X14550542 crossref_primary_10_3390_cosmetics8020042 crossref_primary_10_1007_s00018_019_03371_3 crossref_primary_10_1007_s10555_023_10125_y crossref_primary_10_1007_s11033_022_07516_9 crossref_primary_10_1371_journal_pntd_0007819 crossref_primary_10_36425_rehab64286 crossref_primary_10_1016_j_heliyon_2024_e38688 crossref_primary_10_1016_j_jpha_2023_06_002 crossref_primary_10_1038_s41598_017_04183_w crossref_primary_10_1016_j_ygeno_2025_111106 crossref_primary_10_23736_S0392_9590_19_04250_0 crossref_primary_10_1038_s41598_018_38040_1 crossref_primary_10_1016_j_vesic_2023_100028 crossref_primary_10_1186_scrt346 crossref_primary_10_1016_j_intimp_2022_109260 crossref_primary_10_1016_j_amjms_2019_02_012 crossref_primary_10_1073_pnas_1308887110 crossref_primary_10_1126_scitranslmed_adk1168 crossref_primary_10_1042_BST20220441 crossref_primary_10_1016_j_yjmcc_2015_10_034 crossref_primary_10_1371_journal_pone_0089830 crossref_primary_10_1016_j_jbc_2021_100520 crossref_primary_10_1016_j_transproceed_2024_02_001 crossref_primary_10_1186_s13020_024_00981_3 crossref_primary_10_1007_s00018_013_1289_1 crossref_primary_10_1038_ncomms12313 crossref_primary_10_1161_ATVBAHA_114_304088 crossref_primary_10_1172_JCI86924 crossref_primary_10_1016_j_biopha_2019_109352 crossref_primary_10_23736_S0392_9590_22_04916_1 crossref_primary_10_1016_j_clinthera_2023_08_015 crossref_primary_10_1186_s12915_025_02125_x crossref_primary_10_1016_j_cyto_2017_08_021 crossref_primary_10_1002_JLB_6MR0522_685R crossref_primary_10_1093_eurheartj_ehac686 crossref_primary_10_1038_s41598_020_79927_2 crossref_primary_10_3390_ijms23010533 crossref_primary_10_1016_j_phrs_2021_105563 crossref_primary_10_1016_j_intimp_2024_113904 crossref_primary_10_3390_biomedicines13061425 crossref_primary_10_1097_MOL_0000000000000634 crossref_primary_10_1371_journal_pone_0109024 crossref_primary_10_15829_1560_4071_2019_2_92_98 crossref_primary_10_1016_j_it_2017_03_001 crossref_primary_10_1161_JAHA_119_013793 crossref_primary_10_1016_j_jnutbio_2020_108575 crossref_primary_10_1016_j_smim_2015_07_002 crossref_primary_10_1016_j_intimp_2023_110338 crossref_primary_10_1038_modpathol_2015_156 crossref_primary_10_1016_j_autrev_2018_02_006 crossref_primary_10_1016_j_abb_2015_11_007 crossref_primary_10_1093_cvr_cvy271 crossref_primary_10_1016_j_imbio_2014_09_010 crossref_primary_10_1007_s11010_024_05031_y crossref_primary_10_2217_epi_2016_0152 crossref_primary_10_3892_ijmm_2019_4135 crossref_primary_10_1002_path_5392 crossref_primary_10_1016_j_jcyt_2019_02_002 crossref_primary_10_3109_02713683_2014_943909 crossref_primary_10_1038_srep42723 crossref_primary_10_3389_fimmu_2023_1166487 crossref_primary_10_3390_immuno2020021 |
| Cites_doi | 10.1016/j.jacc.2011.10.852 10.1016/j.cmet.2007.06.010 10.1056/NEJM199901143400207 10.2741/2692 10.1038/nature05894 10.1042/CS20020240 10.1084/jem.20052205 10.1172/JCI29881 10.1172/JCI44490 10.2353/ajpath.2009.080431 10.1016/S1471-4906(02)02302-5 10.4049/jimmunol.0901368 10.1160/TH11-05-0320 10.1016/S0140-6736(06)68770-9 10.1161/01.CIR.90.2.775 10.1371/journal.pone.0008852 10.1161/01.ATV.19.1.54 10.1161/01.CIR.92.3.657 10.1161/CIRCULATIONAHA.110.984146 10.1161/CIRCRESAHA.110.233775 10.1016/j.jacc.2011.01.048 10.1161/01.CIR.89.1.36 10.1369/jhc.2007.950170 10.1161/CIRCRESAHA.109.215715 10.1177/41.10.7504008 10.1016/j.cardiores.2007.06.023 10.1161/ATVBAHA.108.180497 10.1097/MCO.0b013e328347970b 10.1016/j.amjcard.2012.02.050 10.1016/j.cmet.2010.06.008 10.2353/ajpath.2008.070513 10.1016/j.ijcard.2012.03.105 10.1073/pnas.0730843100 10.4049/jimmunol.177.10.7303 10.1136/hrt.2010.205781.49 10.1161/01.ATV.0000229695.68416.76 10.1161/01.ATV.20.5.1262 |
| ContentType | Journal Article |
| Copyright | 2012 Elsevier Ireland Ltd Elsevier Ireland Ltd 2015 INIST-CNRS Copyright © 2012 Elsevier Ireland Ltd. All rights reserved. |
| Copyright_xml | – notice: 2012 Elsevier Ireland Ltd – notice: Elsevier Ireland Ltd – notice: 2015 INIST-CNRS – notice: Copyright © 2012 Elsevier Ireland Ltd. All rights reserved. |
| DBID | 6I. AAFTH FBQ AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7X8 7S9 L.6 |
| DOI | 10.1016/j.atherosclerosis.2012.09.013 |
| DatabaseName | ScienceDirect Open Access Titles Elsevier:ScienceDirect:Open Access AGRIS CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic AGRICOLA AGRICOLA - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic AGRICOLA AGRICOLA - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE AGRICOLA |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1879-1484 |
| EndPage | 468 |
| ExternalDocumentID | 23078881 26619613 10_1016_j_atherosclerosis_2012_09_013 US201500048884 S0021915012006314 1_s2_0_S0021915012006314 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- --K --M .1- .55 .FO .GJ .~1 0R~ 1B1 1P~ 1RT 1~. 1~5 23N 3O- 4.4 457 4G. 53G 5GY 5RE 5VS 7-5 71M 8P~ 9JM AABNK AAEDT AAEDW AAFWJ AAIKJ AAKOC AALRI AAOAW AAQFI AATTM AAXKI AAXUO AAYWO ABBQC ABFNM ABJNI ABLJU ABMAC ABMZM ABOCM ABXDB ACDAQ ACGFS ACIEU ACIUM ACLOT ACRLP ACVFH ADBBV ADCNI ADEZE AEBSH AEIPS AEKER AENEX AEUPX AEVXI AEXQZ AFFNX AFJKZ AFPUW AFRHN AFTJW AFXIZ AGHFR AGUBO AGYEJ AHHHB AIEXJ AIGII AIIUN AIKHN AITUG AJRQY AJUYK AKBMS AKRWK AKYEP ALMA_UNASSIGNED_HOLDINGS AMRAJ ANKPU ANZVX APXCP ASPBG AVWKF AXJTR AZFZN BKOJK BLXMC BNPGV CS3 EBS EFJIC EFKBS EFLBG EJD EO8 EO9 EP2 EP3 F5P FDB FEDTE FGOYB FIRID FNPLU FYGXN G-2 G-Q GBLVA HEB HMK HMO HVGLF HZ~ IHE J1W J5H K-O KOM L7B M27 M41 MO0 N9A O-L O9- OAUVE OA~ OK1 OL0 OZT P-8 P-9 P2P PC. Q38 R2- ROL RPZ SAE SCC SDF SDG SDP SEL SES SEW SPCBC SSH SSZ T5K WUQ X7M Z5R ZGI ZXP ~G- ~HD ~KM AACTN AFCTW AFKWA AJOXV AMFUW NCXOZ RIG 0SF 6I. AAFTH AAIAV ABLVK ABYKQ AHPSJ AJBFU LCYCR ZA5 ABPIF AEQTP FBQ 9DU AAYXX CITATION AGCQF AGRNS IQODW CGR CUY CVF ECM EIF NPM 7X8 7S9 L.6 |
| ID | FETCH-LOGICAL-c747t-459f98a4c40a67b0e816316c9d692384ed5dbf62b0327d42b90ba26b0ee7de2d3 |
| ISICitedReferencesCount | 520 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000311344700055&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 0021-9150 1879-1484 |
| IngestDate | Sun Sep 28 06:42:55 EDT 2025 Thu Oct 02 14:58:27 EDT 2025 Thu Apr 03 06:57:14 EDT 2025 Mon Jul 21 09:14:01 EDT 2025 Tue Nov 18 22:28:44 EST 2025 Sat Nov 29 06:31:13 EST 2025 Wed Dec 27 19:16:15 EST 2023 Fri Feb 23 02:28:14 EST 2024 Sun Feb 23 10:19:10 EST 2025 Tue Oct 14 19:27:08 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Keywords | Innate immunity Foam cell Macrophages Coronary artery disease Human pathology Human Cardiovascular disease Coronary heart disease Immunity Vascular disease Anatomic pathology Atherosclerosis Macrophage |
| Language | English |
| License | http://www.elsevier.com/open-access/userlicense/1.0 https://www.elsevier.com/tdm/userlicense/1.0 https://www.elsevier.com/open-access/userlicense/1.0 CC BY 4.0 Copyright © 2012 Elsevier Ireland Ltd. All rights reserved. |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c747t-459f98a4c40a67b0e816316c9d692384ed5dbf62b0327d42b90ba26b0ee7de2d3 |
| Notes | http://dx.doi.org/10.1016/j.atherosclerosis.2012.09.013 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://www.clinicalkey.com/#!/content/1-s2.0-S0021915012006314 |
| PMID | 23078881 |
| PQID | 1179548196 |
| PQPubID | 23479 |
| PageCount | 8 |
| ParticipantIDs | proquest_miscellaneous_1672089357 proquest_miscellaneous_1179548196 pubmed_primary_23078881 pascalfrancis_primary_26619613 crossref_primary_10_1016_j_atherosclerosis_2012_09_013 crossref_citationtrail_10_1016_j_atherosclerosis_2012_09_013 fao_agris_US201500048884 elsevier_sciencedirect_doi_10_1016_j_atherosclerosis_2012_09_013 elsevier_clinicalkeyesjournals_1_s2_0_S0021915012006314 elsevier_clinicalkey_doi_10_1016_j_atherosclerosis_2012_09_013 |
| PublicationCentury | 2000 |
| PublicationDate | 2012-12-01 |
| PublicationDateYYYYMMDD | 2012-12-01 |
| PublicationDate_xml | – month: 12 year: 2012 text: 2012-12-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | Amsterdam |
| PublicationPlace_xml | – name: Amsterdam – name: Ireland |
| PublicationTitle | Atherosclerosis |
| PublicationTitleAlternate | Atherosclerosis |
| PublicationYear | 2012 |
| Publisher | Elsevier Ireland Ltd Elsevier |
| Publisher_xml | – name: Elsevier Ireland Ltd – name: Elsevier |
| References | Martinez, Gordon, Locati, Mantovani (bib6) 2006 Nov. 15; 177 Younge JO, Damen NL, van Domburg RT, Pedersen SS. Obesity, health status, and 7-year mortality in percutaneous coronary intervention: in search of an explanation for the obesity paradox. Int J Cardiol 2012 Lopez, Mathers, Ezzati, Jamison, Murray (bib2) 2006 May 27; 367 Feig, Parathath, Rong (bib35) 2011 Mar. 7; 123 Odegaard, Ricardo-Gonzalez, Goforth (bib30) 2007 May 21; 447 Chinetti-Gbaguidi, Baron, Bouhlel (bib24) 2011 Apr. 14; 108 Ross (bib1) 1999 Jan. 14; 340 Hirata, Tabata, Kurobe (bib39) 2011 Jul. 12; 58 Khallou-Laschet, Varthaman, Fornasa (bib9) 2010 Jan. 25; 5 Pasterkamp, Schoneveld, van der Wal (bib22) 1999 Jan. 1; 19 Clark, Chyu, Horwich (bib33) 2012 Jul. 1; 110 Waldo, Li, Buono (bib11) 2008 Apr.; 172 van der Wal, Becker, van der Loos, Das (bib4) 1994 Jan.; 89 Wolfs, Donners, de Winther (bib15) 2011; 106 Moulton, Vakili, Zurakowski (bib29) 2003 Apr. 15; 100 Falk, Shah, Fuster (bib36) 1995 Aug. 1; 92 Virmani, Kolodgie, Burke, Farb, Schwartz (bib18) 2000 May; 20 Gleissner, Shaked, Little, Ley (bib14) 2010 Apr. 21; 184 Kadl, Meher, Sharma (bib13) 2010 Sep. 17; 107 Mantovani, Garlanda, Locati (bib16) 2009 Sep. 16; 29 Boyle, Harrington, Piper (bib21) 2009 Mar.; 174 Bouhlel, Derudas, Rigamonti (bib10) 2007 Aug.; 6 Poston, Hussain (bib26) 1993 Oct.; 41 van der Loos (bib19) 2008 Apr.; 56 Papaspyridonos, Smith, Burnand (bib20) 2006 Aug.; 26 Anyfanti, Doumas, Gavriilaki, Triantafyllou, Nikolaidou (bib32) 2012 Mantovani, Sozzani, Locati, Allavena, Sica (bib8) 2002 Nov.; 23 Sindrilaru, Peters, Wieschalka (bib27) 2011 Mar. 1; 121 Morris, Singer, Lumeng (bib31) 2011 Jul.; 14 Galkina, Kadl, Sanders, Varughese, Sarembock, Ley (bib23) 2006 May 15; 203 Shalhoub, Cross, Allin, Essex, Davies, Monaco (bib38) 2010 Aug. 26; 96 . Martinez, Sica, Mantovani, Locati (bib5) 2008; 13 Finn, Nakano, Polavarapu (bib12) 2012 Jan. 10; 59 Shalhoub, Falck-Hansen, Davies, Monaco (bib25) 2011; 8 Duffield (bib37) 2003 Jan.; 104 Maiellaro, Taylor (bib28) 2007 Sep. 1; 75 Moreno, Falk, Palacios, Newell, Fuster, Fallon (bib3) 1994 Aug.; 90 Lumeng, Bodzin, Saltiel (bib7) 2007 Jan. 2; 117 Goossens, Gijbels, Zernecke (bib17) 2010 Aug. 4; 12 Goossens (10.1016/j.atherosclerosis.2012.09.013_bib17) 2010; 12 Moulton (10.1016/j.atherosclerosis.2012.09.013_bib29) 2003; 100 Clark (10.1016/j.atherosclerosis.2012.09.013_bib33) 2012; 110 Papaspyridonos (10.1016/j.atherosclerosis.2012.09.013_bib20) 2006; 26 Shalhoub (10.1016/j.atherosclerosis.2012.09.013_bib38) 2010; 96 Pasterkamp (10.1016/j.atherosclerosis.2012.09.013_bib22) 1999; 19 Morris (10.1016/j.atherosclerosis.2012.09.013_bib31) 2011; 14 Feig (10.1016/j.atherosclerosis.2012.09.013_bib35) 2011; 123 Lumeng (10.1016/j.atherosclerosis.2012.09.013_bib7) 2007; 117 Maiellaro (10.1016/j.atherosclerosis.2012.09.013_bib28) 2007; 75 Khallou-Laschet (10.1016/j.atherosclerosis.2012.09.013_bib9) 2010; 5 Kadl (10.1016/j.atherosclerosis.2012.09.013_bib13) 2010; 107 Gleissner (10.1016/j.atherosclerosis.2012.09.013_bib14) 2010; 184 Waldo (10.1016/j.atherosclerosis.2012.09.013_bib11) 2008; 172 10.1016/j.atherosclerosis.2012.09.013_bib34 van der Wal (10.1016/j.atherosclerosis.2012.09.013_bib4) 1994; 89 Bouhlel (10.1016/j.atherosclerosis.2012.09.013_bib10) 2007; 6 Poston (10.1016/j.atherosclerosis.2012.09.013_bib26) 1993; 41 Lopez (10.1016/j.atherosclerosis.2012.09.013_bib2) 2006; 367 Hirata (10.1016/j.atherosclerosis.2012.09.013_bib39) 2011; 58 Duffield (10.1016/j.atherosclerosis.2012.09.013_bib37) 2003; 104 Ross (10.1016/j.atherosclerosis.2012.09.013_bib1) 1999; 340 Chinetti-Gbaguidi (10.1016/j.atherosclerosis.2012.09.013_bib24) 2011; 108 Finn (10.1016/j.atherosclerosis.2012.09.013_bib12) 2012; 59 Anyfanti (10.1016/j.atherosclerosis.2012.09.013_bib32) 2012 van der Loos (10.1016/j.atherosclerosis.2012.09.013_bib19) 2008; 56 Sindrilaru (10.1016/j.atherosclerosis.2012.09.013_bib27) 2011; 121 Martinez (10.1016/j.atherosclerosis.2012.09.013_bib5) 2008; 13 Odegaard (10.1016/j.atherosclerosis.2012.09.013_bib30) 2007; 447 Virmani (10.1016/j.atherosclerosis.2012.09.013_bib18) 2000; 20 Mantovani (10.1016/j.atherosclerosis.2012.09.013_bib8) 2002; 23 Moreno (10.1016/j.atherosclerosis.2012.09.013_bib3) 1994; 90 Galkina (10.1016/j.atherosclerosis.2012.09.013_bib23) 2006; 203 Shalhoub (10.1016/j.atherosclerosis.2012.09.013_bib25) 2011; 8 Wolfs (10.1016/j.atherosclerosis.2012.09.013_bib15) 2011; 106 Mantovani (10.1016/j.atherosclerosis.2012.09.013_bib16) 2009; 29 Falk (10.1016/j.atherosclerosis.2012.09.013_bib36) 1995; 92 Martinez (10.1016/j.atherosclerosis.2012.09.013_bib6) 2006; 177 Boyle (10.1016/j.atherosclerosis.2012.09.013_bib21) 2009; 174 |
| References_xml | – volume: 340 start-page: 115 year: 1999 Jan. 14 end-page: 126 ident: bib1 article-title: Atherosclerosis – an inflammatory disease publication-title: N Engl J Med – volume: 13 start-page: 453 year: 2008 end-page: 461 ident: bib5 article-title: Macrophage activation and polarization publication-title: Front Biosci – volume: 447 start-page: 1116 year: 2007 May 21 end-page: 1120 ident: bib30 article-title: Macrophage-specific PPARγ controls alternative activation and improves insulin resistance publication-title: Nature – volume: 106 start-page: 763 year: 2011 end-page: 771 ident: bib15 article-title: Differentiation factors and cytokines in the atherosclerotic plaque micro-environment as a trigger for macrophage polarisation publication-title: Thromb Haemost – volume: 58 start-page: 248 year: 2011 Jul. 12 end-page: 255 ident: bib39 article-title: Coronary atherosclerosis is associated with macrophage polarization in epicardial adipose tissue publication-title: J Am Coll Cardiol – year: 2012 ident: bib32 article-title: More fuel in the obesity paradox debate publication-title: Int J Obes – volume: 14 start-page: 341 year: 2011 Jul. end-page: 346 ident: bib31 article-title: Adipose tissue macrophages: phenotypic plasticity and diversity in lean and obese states publication-title: Curr Opin Clin Nutr Metab Care – volume: 107 start-page: 737 year: 2010 Sep. 17 end-page: 746 ident: bib13 article-title: Identification of a novel macrophage phenotype that develops in response to atherogenic phospholipids via Nrf2 publication-title: Circ Res – volume: 92 start-page: 657 year: 1995 Aug. 1 end-page: 671 ident: bib36 article-title: Coronary plaque disruption publication-title: Circulation – volume: 117 start-page: 175 year: 2007 Jan. 2 end-page: 184 ident: bib7 article-title: Obesity induces a phenotypic switch in adipose tissue macrophage polarization publication-title: J Clin Invest – volume: 110 start-page: 77 year: 2012 Jul. 1 end-page: 82 ident: bib33 article-title: The obesity paradox in men versus women with systolic heart failure publication-title: Am J Cardiol – volume: 59 start-page: 166 year: 2012 Jan. 10 end-page: 177 ident: bib12 article-title: Hemoglobin directs macrophage differentiation and prevents foam cell formation in human atherosclerotic plaques publication-title: J Am Coll Cardiol – volume: 8 start-page: 9 year: 2011 ident: bib25 article-title: Innate immunity and monocyte-macrophage activation in atherosclerosis publication-title: J Inflamm – volume: 56 start-page: 313 year: 2008 Apr. end-page: 328 ident: bib19 article-title: Multiple immunoenzyme staining: methods and visualizations for the observation with spectral imaging publication-title: J Histochem Cytochem – volume: 20 start-page: 1262 year: 2000 May end-page: 1275 ident: bib18 article-title: Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions publication-title: Arterioscler Thromb Vasc Biol – volume: 177 start-page: 7303 year: 2006 Nov. 15 end-page: 7311 ident: bib6 article-title: Transcriptional profiling of the human monocyte-to-macrophage differentiation and polarization: new molecules and patterns of gene expression publication-title: J Immunol – volume: 75 start-page: 640 year: 2007 Sep. 1 end-page: 648 ident: bib28 article-title: The role of the adventitia in vascular inflammation publication-title: Cardiovasc Res – volume: 123 start-page: 989 year: 2011 Mar. 7 end-page: 998 ident: bib35 article-title: Reversal of hyperlipidemia with a genetic switch favorably affects the content and inflammatory state of macrophages in atherosclerotic plaques publication-title: Circulation – volume: 5 start-page: e8852 year: 2010 Jan. 25 ident: bib9 article-title: Macrophage plasticity in experimental atherosclerosis publication-title: PLoS ONE – volume: 19 start-page: 54 year: 1999 Jan. 1 end-page: 58 ident: bib22 article-title: Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries publication-title: Arterioscler Thromb Vasc Biol – volume: 203 start-page: 1273 year: 2006 May 15 end-page: 1282 ident: bib23 article-title: Lymphocyte recruitment into the aortic wall before and during development of atherosclerosis is partially L-selectin dependent publication-title: J Exp Med – volume: 367 start-page: 1747 year: 2006 May 27 end-page: 1757 ident: bib2 article-title: Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data publication-title: Lancet – volume: 108 start-page: 985 year: 2011 Apr. 14 end-page: 995 ident: bib24 article-title: Human atherosclerotic plaque alternative macrophages display low cholesterol handling but high phagocytosis because of distinct activities of the PPAR and LXR pathways publication-title: Circ Res – volume: 96 start-page: e23 year: 2010 Aug. 26 end-page: 3 ident: bib38 article-title: BAS/BSCR36 cytokine profiling in culture reveals a predominance of M1 macrophage polarisation in symptomatic carotid plaques publication-title: Heart – volume: 90 start-page: 775 year: 1994 Aug. end-page: 778 ident: bib3 article-title: Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture publication-title: Circulation – reference: . – volume: 104 start-page: 27 year: 2003 Jan. end-page: 38 ident: bib37 article-title: The inflammatory macrophage: a story of Jekyll and Hyde publication-title: Clin Sci – volume: 89 start-page: 36 year: 1994 Jan. end-page: 44 ident: bib4 article-title: Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology publication-title: Circulation – volume: 29 start-page: 1419 year: 2009 Sep. 16 end-page: 1423 ident: bib16 article-title: Macrophage diversity and polarization in atherosclerosis: a question of balance publication-title: Arterioscler Thromb Vasc Biol – volume: 12 start-page: 142 year: 2010 Aug. 4 end-page: 153 ident: bib17 article-title: Myeloid type i interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions publication-title: Cell Metab – volume: 172 start-page: 1112 year: 2008 Apr. end-page: 1126 ident: bib11 article-title: Heterogeneity of human macrophages in culture and in atherosclerotic plaques publication-title: Am J Pathol – volume: 26 start-page: 1837 year: 2006 Aug. end-page: 1844 ident: bib20 article-title: Novel candidate genes in unstable areas of human atherosclerotic plaques publication-title: Arterioscler Thromb Vasc Biol – volume: 6 start-page: 137 year: 2007 Aug. end-page: 143 ident: bib10 article-title: PPARγ activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties publication-title: Cell Metab – volume: 100 start-page: 4736 year: 2003 Apr. 15 end-page: 4741 ident: bib29 article-title: Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis publication-title: Proc Natl Acad Sci USA – volume: 23 start-page: 549 year: 2002 Nov. end-page: 555 ident: bib8 article-title: Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes publication-title: Trends Immunol – volume: 184 start-page: 4810 year: 2010 Apr. 21 end-page: 4818 ident: bib14 article-title: CXC chemokine ligand 4 induces a unique transcriptome in monocyte-derived macrophages publication-title: J Immunol – reference: Younge JO, Damen NL, van Domburg RT, Pedersen SS. Obesity, health status, and 7-year mortality in percutaneous coronary intervention: in search of an explanation for the obesity paradox. Int J Cardiol 2012, – volume: 174 start-page: 1097 year: 2009 Mar. end-page: 1108 ident: bib21 article-title: Coronary intraplaque hemorrhage evokes a novel atheroprotective macrophage phenotype publication-title: Am J Pathol – volume: 41 start-page: 1503 year: 1993 Oct. end-page: 1512 ident: bib26 article-title: The immunohistochemical heterogeneity of atheroma macrophages: comparison with lymphoid tissues suggests that recently blood-derived macrophages can be distinguished from longer-resident cells publication-title: J Histochem Cytochem – volume: 121 start-page: 985 year: 2011 Mar. 1 end-page: 997 ident: bib27 article-title: An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice publication-title: J Clin Invest – volume: 59 start-page: 166 issue: 2 year: 2012 ident: 10.1016/j.atherosclerosis.2012.09.013_bib12 article-title: Hemoglobin directs macrophage differentiation and prevents foam cell formation in human atherosclerotic plaques publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2011.10.852 – volume: 6 start-page: 137 issue: 2 year: 2007 ident: 10.1016/j.atherosclerosis.2012.09.013_bib10 article-title: PPARγ activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties publication-title: Cell Metab doi: 10.1016/j.cmet.2007.06.010 – volume: 8 start-page: 9 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib25 article-title: Innate immunity and monocyte-macrophage activation in atherosclerosis publication-title: J Inflamm – volume: 340 start-page: 115 issue: 2 year: 1999 ident: 10.1016/j.atherosclerosis.2012.09.013_bib1 article-title: Atherosclerosis – an inflammatory disease publication-title: N Engl J Med doi: 10.1056/NEJM199901143400207 – volume: 13 start-page: 453 year: 2008 ident: 10.1016/j.atherosclerosis.2012.09.013_bib5 article-title: Macrophage activation and polarization publication-title: Front Biosci doi: 10.2741/2692 – volume: 447 start-page: 1116 issue: 7148 year: 2007 ident: 10.1016/j.atherosclerosis.2012.09.013_bib30 article-title: Macrophage-specific PPARγ controls alternative activation and improves insulin resistance publication-title: Nature doi: 10.1038/nature05894 – volume: 104 start-page: 27 issue: 1 year: 2003 ident: 10.1016/j.atherosclerosis.2012.09.013_bib37 article-title: The inflammatory macrophage: a story of Jekyll and Hyde publication-title: Clin Sci doi: 10.1042/CS20020240 – volume: 203 start-page: 1273 issue: 5 year: 2006 ident: 10.1016/j.atherosclerosis.2012.09.013_bib23 article-title: Lymphocyte recruitment into the aortic wall before and during development of atherosclerosis is partially L-selectin dependent publication-title: J Exp Med doi: 10.1084/jem.20052205 – volume: 117 start-page: 175 issue: 1 year: 2007 ident: 10.1016/j.atherosclerosis.2012.09.013_bib7 article-title: Obesity induces a phenotypic switch in adipose tissue macrophage polarization publication-title: J Clin Invest doi: 10.1172/JCI29881 – volume: 121 start-page: 985 issue: 3 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib27 article-title: An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice publication-title: J Clin Invest doi: 10.1172/JCI44490 – volume: 174 start-page: 1097 issue: 3 year: 2009 ident: 10.1016/j.atherosclerosis.2012.09.013_bib21 article-title: Coronary intraplaque hemorrhage evokes a novel atheroprotective macrophage phenotype publication-title: Am J Pathol doi: 10.2353/ajpath.2009.080431 – volume: 23 start-page: 549 issue: 11 year: 2002 ident: 10.1016/j.atherosclerosis.2012.09.013_bib8 article-title: Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes publication-title: Trends Immunol doi: 10.1016/S1471-4906(02)02302-5 – volume: 184 start-page: 4810 issue: 9 year: 2010 ident: 10.1016/j.atherosclerosis.2012.09.013_bib14 article-title: CXC chemokine ligand 4 induces a unique transcriptome in monocyte-derived macrophages publication-title: J Immunol doi: 10.4049/jimmunol.0901368 – volume: 106 start-page: 763 issue: 5 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib15 article-title: Differentiation factors and cytokines in the atherosclerotic plaque micro-environment as a trigger for macrophage polarisation publication-title: Thromb Haemost doi: 10.1160/TH11-05-0320 – volume: 367 start-page: 1747 issue: 9524 year: 2006 ident: 10.1016/j.atherosclerosis.2012.09.013_bib2 article-title: Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data publication-title: Lancet doi: 10.1016/S0140-6736(06)68770-9 – volume: 90 start-page: 775 issue: 2 year: 1994 ident: 10.1016/j.atherosclerosis.2012.09.013_bib3 article-title: Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture publication-title: Circulation doi: 10.1161/01.CIR.90.2.775 – volume: 5 start-page: e8852 issue: 1 year: 2010 ident: 10.1016/j.atherosclerosis.2012.09.013_bib9 article-title: Macrophage plasticity in experimental atherosclerosis publication-title: PLoS ONE doi: 10.1371/journal.pone.0008852 – volume: 19 start-page: 54 issue: 1 year: 1999 ident: 10.1016/j.atherosclerosis.2012.09.013_bib22 article-title: Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/01.ATV.19.1.54 – volume: 92 start-page: 657 issue: 3 year: 1995 ident: 10.1016/j.atherosclerosis.2012.09.013_bib36 article-title: Coronary plaque disruption publication-title: Circulation doi: 10.1161/01.CIR.92.3.657 – year: 2012 ident: 10.1016/j.atherosclerosis.2012.09.013_bib32 article-title: More fuel in the obesity paradox debate publication-title: Int J Obes – volume: 123 start-page: 989 issue: 9 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib35 article-title: Reversal of hyperlipidemia with a genetic switch favorably affects the content and inflammatory state of macrophages in atherosclerotic plaques publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.110.984146 – volume: 108 start-page: 985 issue: 8 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib24 article-title: Human atherosclerotic plaque alternative macrophages display low cholesterol handling but high phagocytosis because of distinct activities of the PPAR and LXR pathways publication-title: Circ Res doi: 10.1161/CIRCRESAHA.110.233775 – volume: 58 start-page: 248 issue: 3 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib39 article-title: Coronary atherosclerosis is associated with macrophage polarization in epicardial adipose tissue publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2011.01.048 – volume: 89 start-page: 36 issue: 1 year: 1994 ident: 10.1016/j.atherosclerosis.2012.09.013_bib4 article-title: Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology publication-title: Circulation doi: 10.1161/01.CIR.89.1.36 – volume: 56 start-page: 313 issue: 4 year: 2008 ident: 10.1016/j.atherosclerosis.2012.09.013_bib19 article-title: Multiple immunoenzyme staining: methods and visualizations for the observation with spectral imaging publication-title: J Histochem Cytochem doi: 10.1369/jhc.2007.950170 – volume: 107 start-page: 737 issue: 6 year: 2010 ident: 10.1016/j.atherosclerosis.2012.09.013_bib13 article-title: Identification of a novel macrophage phenotype that develops in response to atherogenic phospholipids via Nrf2 publication-title: Circ Res doi: 10.1161/CIRCRESAHA.109.215715 – volume: 41 start-page: 1503 issue: 10 year: 1993 ident: 10.1016/j.atherosclerosis.2012.09.013_bib26 article-title: The immunohistochemical heterogeneity of atheroma macrophages: comparison with lymphoid tissues suggests that recently blood-derived macrophages can be distinguished from longer-resident cells publication-title: J Histochem Cytochem doi: 10.1177/41.10.7504008 – volume: 75 start-page: 640 issue: 4 year: 2007 ident: 10.1016/j.atherosclerosis.2012.09.013_bib28 article-title: The role of the adventitia in vascular inflammation publication-title: Cardiovasc Res doi: 10.1016/j.cardiores.2007.06.023 – volume: 29 start-page: 1419 issue: 10 year: 2009 ident: 10.1016/j.atherosclerosis.2012.09.013_bib16 article-title: Macrophage diversity and polarization in atherosclerosis: a question of balance publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.108.180497 – volume: 14 start-page: 341 issue: 4 year: 2011 ident: 10.1016/j.atherosclerosis.2012.09.013_bib31 article-title: Adipose tissue macrophages: phenotypic plasticity and diversity in lean and obese states publication-title: Curr Opin Clin Nutr Metab Care doi: 10.1097/MCO.0b013e328347970b – volume: 110 start-page: 77 issue: 1 year: 2012 ident: 10.1016/j.atherosclerosis.2012.09.013_bib33 article-title: The obesity paradox in men versus women with systolic heart failure publication-title: Am J Cardiol doi: 10.1016/j.amjcard.2012.02.050 – volume: 12 start-page: 142 issue: 2 year: 2010 ident: 10.1016/j.atherosclerosis.2012.09.013_bib17 article-title: Myeloid type i interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions publication-title: Cell Metab doi: 10.1016/j.cmet.2010.06.008 – volume: 172 start-page: 1112 issue: 4 year: 2008 ident: 10.1016/j.atherosclerosis.2012.09.013_bib11 article-title: Heterogeneity of human macrophages in culture and in atherosclerotic plaques publication-title: Am J Pathol doi: 10.2353/ajpath.2008.070513 – ident: 10.1016/j.atherosclerosis.2012.09.013_bib34 doi: 10.1016/j.ijcard.2012.03.105 – volume: 100 start-page: 4736 issue: 8 year: 2003 ident: 10.1016/j.atherosclerosis.2012.09.013_bib29 article-title: Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0730843100 – volume: 177 start-page: 7303 issue: 10 year: 2006 ident: 10.1016/j.atherosclerosis.2012.09.013_bib6 article-title: Transcriptional profiling of the human monocyte-to-macrophage differentiation and polarization: new molecules and patterns of gene expression publication-title: J Immunol doi: 10.4049/jimmunol.177.10.7303 – volume: 96 start-page: e23 issue: 17 year: 2010 ident: 10.1016/j.atherosclerosis.2012.09.013_bib38 article-title: BAS/BSCR36 cytokine profiling in culture reveals a predominance of M1 macrophage polarisation in symptomatic carotid plaques publication-title: Heart doi: 10.1136/hrt.2010.205781.49 – volume: 26 start-page: 1837 issue: 8 year: 2006 ident: 10.1016/j.atherosclerosis.2012.09.013_bib20 article-title: Novel candidate genes in unstable areas of human atherosclerotic plaques publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/01.ATV.0000229695.68416.76 – volume: 20 start-page: 1262 issue: 5 year: 2000 ident: 10.1016/j.atherosclerosis.2012.09.013_bib18 article-title: Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/01.ATV.20.5.1262 |
| SSID | ssj0004718 |
| Score | 2.582116 |
| Snippet | Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and spatial... Abstract Objective Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the... OBJECTIVE: Macrophages are decisive in the chronic inflammatory processes that drive atherogenesis. The purpose of this study was to explore the presence and... |
| SourceID | proquest pubmed pascalfrancis crossref fao elsevier |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 461 |
| SubjectTerms | Adventitia Adventitia - immunology Adventitia - pathology Aged Aged, 80 and over analysis atherogenesis atherosclerosis Atherosclerosis (general aspects, experimental research) Biological and medical sciences Biomarkers Biomarkers - analysis Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular Cardiovascular system Carotid Arteries Carotid Arteries - immunology Carotid Arteries - pathology Carotid Artery Diseases Carotid Artery Diseases - genetics Carotid Artery Diseases - immunology Carotid Artery Diseases - pathology classification Coronary artery disease Disease Progression Female Fibrosis Foam cell Gene Expression Profiling Gene Expression Regulation genetics hemorrhage Human pathology Humans Immunohistochemistry immunology Inflammation Mediators Inflammation Mediators - analysis Innate immunity Macrophages Macrophages - classification Macrophages - immunology Macrophages - pathology Male Medical sciences pathology Pharmacology. Drug treatments Plaque, Atherosclerotic RNA, Messenger RNA, Messenger - analysis Rupture, Spontaneous Severity of Illness Index transcription (genetics) Transcriptome transcriptomics Vasodilator agents. Cerebral vasodilators |
| Title | Distribution of macrophage polarization markers in human atherosclerosis |
| URI | https://www.clinicalkey.com/#!/content/1-s2.0-S0021915012006314 https://www.clinicalkey.es/playcontent/1-s2.0-S0021915012006314 https://dx.doi.org/10.1016/j.atherosclerosis.2012.09.013 https://www.ncbi.nlm.nih.gov/pubmed/23078881 https://www.proquest.com/docview/1179548196 https://www.proquest.com/docview/1672089357 |
| Volume | 225 |
| WOSCitedRecordID | wos000311344700055&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVESC databaseName: Elsevier SD Freedom Collection Journals 2021 customDbUrl: eissn: 1879-1484 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0004718 issn: 0021-9150 databaseCode: AIEXJ dateStart: 19950106 isFulltext: true titleUrlDefault: https://www.sciencedirect.com providerName: Elsevier |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtR3ZbtNAcJW0qOIFcTcckZGANyN74-x6JYQIkFKiNiA1QXlb-VgXp5Ed4rTqF_DdzNhrOw1plT7wYkXrvbIznmvnIOQ1i1jHBypnMoWmm0C4QAddzwyA9_o08oBlBHmxCT4cupOJ-NFo_CljYS5mPEncy0sx_6-ghjYANobO3gLc1aTQAL8B6PAEsMNzK8B_wVS4uopVfnvuYZWuX-ibM0c9VgdeQvviDKN340QX6stlwTSD6eAZZ6tia2_Dq9wZGO_ZP7HTAu6DPMq6Rrev8dQH1qtDgnDNQX0LhXFTmMfip5pp0nfiZWdxxSWO0diihwbpqnHCpiuOHgU9dbkw7SJdKbCbDW2aCNMi_FljG10hqU6RrP0fUl9YHabv1g4HvfVonrq2iHG9mmJ7-F0ejI-O5Kg_Gb2d_zax-hje0utSLE2yS3lXAHXc7X3rTwZ1hC3PLcXV1vfIm9pT8IYdXCftNCMvRTdcL4MvMSpKqFyv4-Syzug-uaeVFKNXINcD0lDJQ7J3rN0wHpHDVRwz0sioccxYxTFD45gRJ0aOY8ban3hMxgf90edDU5fkMAPQO5em0xWRcD0ncCyPcd9SLsjzNgtEyEBTcB0VdkM_YtS3OpSHDvWF5XuUQUfFQ0XDzhOyk6SJ2icG86kKOxF3XCQLji1CjytgthG3KPeF2yLvy6OTgc5Xj2VTZrJ0TJzKtU1LPHlpCQkn3yKsGj4vErdsO_BDCSdZRicDP5WAd9tOwDdNoDJNJDJpyww6S3SUsAVoZDba9Tq20yIfq5FaAC4E29ssvg-oJb1TEBHk-ISiQTPn0i7M3r6Cb9WxoIwuGI59VSKgBCaDN4deotLzDCsCYGJI6HVDH8apBdpPl7fI0wJ76xVAkoAt2M-2WOE5uVtTkhdkZ7k4Vy_JneBiGWeLNmnyidvWn-dfBaoNHQ |
| linkProvider | Elsevier |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Distribution+of+macrophage+polarization+markers+in+human+atherosclerosis&rft.jtitle=Atherosclerosis&rft.au=St%C3%B6ger%2C+J+Lauran&rft.au=Gijbels%2C+Marion+J+J&rft.au=van+der+Velden%2C+Saskia&rft.au=Manca%2C+Marco&rft.date=2012-12-01&rft.issn=1879-1484&rft.eissn=1879-1484&rft.volume=225&rft.issue=2&rft.spage=461&rft_id=info:doi/10.1016%2Fj.atherosclerosis.2012.09.013&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_m | http://cvtisr.summon.serialssolutions.com/2.0.0/image/custom?url=https%3A%2F%2Fcdn.clinicalkey.com%2Fck-thumbnails%2F00219150%2FS0021915012X00121%2Fcov150h.gif |