Sugar-based amphiphilic nanoparticles arrest atherosclerosis in vivo

Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a focal trigger of chronic coronary, intracranial, and peripheral arterial diseases, which together account for the leading causes of death worldwide. Although the directed treatment of atherosclerotic plaques remai...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS Vol. 112; no. 9; p. 2693
Main Authors: Lewis, Daniel R, Petersen, Latrisha K, York, Adam W, Zablocki, Kyle R, Joseph, Laurie B, Kholodovych, Vladyslav, Prud'homme, Robert K, Uhrich, Kathryn E, Moghe, Prabhas V
Format: Journal Article
Language:English
Published: United States 03.03.2015
Subjects:
ISSN:1091-6490, 1091-6490
Online Access:Get more information
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a focal trigger of chronic coronary, intracranial, and peripheral arterial diseases, which together account for the leading causes of death worldwide. Although the directed treatment of atherosclerotic plaques remains elusive, macrophages are a natural target for new interventions because they are recruited to lipid-rich lesions, actively internalize modified lipids, and convert to foam cells with diseased phenotypes. In this work, we present a nanomedicine platform to counteract plaque development based on two building blocks: first, at the single macrophage level, sugar-based amphiphilic macromolecules (AMs) were designed to competitively block oxidized lipid uptake via scavenger receptors on macrophages; second, for sustained lesion-level intervention, AMs were fabricated into serum-stable core/shell nanoparticles (NPs) to rapidly associate with plaques and inhibit disease progression in vivo. An AM library was designed and fabricated into NP compositions that showed high binding and down-regulation of both MSR1 and CD36 scavenger receptors, yielding minimal accumulation of oxidized lipids. When intravenously administered to a mouse model of cardiovascular disease, these AM NPs showed a pronounced increase in lesion association compared with the control nanoparticles, causing a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts, and overall plaque occlusion. Thus, synthetic macromolecules configured as NPs are not only effectively mobilized to lipid-rich lesions but can also be deployed to counteract atheroinflammatory vascular diseases, highlighting the promise of nanomedicines for hyperlipidemic and metabolic syndromes.
AbstractList Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a focal trigger of chronic coronary, intracranial, and peripheral arterial diseases, which together account for the leading causes of death worldwide. Although the directed treatment of atherosclerotic plaques remains elusive, macrophages are a natural target for new interventions because they are recruited to lipid-rich lesions, actively internalize modified lipids, and convert to foam cells with diseased phenotypes. In this work, we present a nanomedicine platform to counteract plaque development based on two building blocks: first, at the single macrophage level, sugar-based amphiphilic macromolecules (AMs) were designed to competitively block oxidized lipid uptake via scavenger receptors on macrophages; second, for sustained lesion-level intervention, AMs were fabricated into serum-stable core/shell nanoparticles (NPs) to rapidly associate with plaques and inhibit disease progression in vivo. An AM library was designed and fabricated into NP compositions that showed high binding and down-regulation of both MSR1 and CD36 scavenger receptors, yielding minimal accumulation of oxidized lipids. When intravenously administered to a mouse model of cardiovascular disease, these AM NPs showed a pronounced increase in lesion association compared with the control nanoparticles, causing a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts, and overall plaque occlusion. Thus, synthetic macromolecules configured as NPs are not only effectively mobilized to lipid-rich lesions but can also be deployed to counteract atheroinflammatory vascular diseases, highlighting the promise of nanomedicines for hyperlipidemic and metabolic syndromes.
Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a focal trigger of chronic coronary, intracranial, and peripheral arterial diseases, which together account for the leading causes of death worldwide. Although the directed treatment of atherosclerotic plaques remains elusive, macrophages are a natural target for new interventions because they are recruited to lipid-rich lesions, actively internalize modified lipids, and convert to foam cells with diseased phenotypes. In this work, we present a nanomedicine platform to counteract plaque development based on two building blocks: first, at the single macrophage level, sugar-based amphiphilic macromolecules (AMs) were designed to competitively block oxidized lipid uptake via scavenger receptors on macrophages; second, for sustained lesion-level intervention, AMs were fabricated into serum-stable core/shell nanoparticles (NPs) to rapidly associate with plaques and inhibit disease progression in vivo. An AM library was designed and fabricated into NP compositions that showed high binding and down-regulation of both MSR1 and CD36 scavenger receptors, yielding minimal accumulation of oxidized lipids. When intravenously administered to a mouse model of cardiovascular disease, these AM NPs showed a pronounced increase in lesion association compared with the control nanoparticles, causing a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts, and overall plaque occlusion. Thus, synthetic macromolecules configured as NPs are not only effectively mobilized to lipid-rich lesions but can also be deployed to counteract atheroinflammatory vascular diseases, highlighting the promise of nanomedicines for hyperlipidemic and metabolic syndromes.Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a focal trigger of chronic coronary, intracranial, and peripheral arterial diseases, which together account for the leading causes of death worldwide. Although the directed treatment of atherosclerotic plaques remains elusive, macrophages are a natural target for new interventions because they are recruited to lipid-rich lesions, actively internalize modified lipids, and convert to foam cells with diseased phenotypes. In this work, we present a nanomedicine platform to counteract plaque development based on two building blocks: first, at the single macrophage level, sugar-based amphiphilic macromolecules (AMs) were designed to competitively block oxidized lipid uptake via scavenger receptors on macrophages; second, for sustained lesion-level intervention, AMs were fabricated into serum-stable core/shell nanoparticles (NPs) to rapidly associate with plaques and inhibit disease progression in vivo. An AM library was designed and fabricated into NP compositions that showed high binding and down-regulation of both MSR1 and CD36 scavenger receptors, yielding minimal accumulation of oxidized lipids. When intravenously administered to a mouse model of cardiovascular disease, these AM NPs showed a pronounced increase in lesion association compared with the control nanoparticles, causing a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts, and overall plaque occlusion. Thus, synthetic macromolecules configured as NPs are not only effectively mobilized to lipid-rich lesions but can also be deployed to counteract atheroinflammatory vascular diseases, highlighting the promise of nanomedicines for hyperlipidemic and metabolic syndromes.
Author Joseph, Laurie B
Prud'homme, Robert K
Kholodovych, Vladyslav
Moghe, Prabhas V
Lewis, Daniel R
York, Adam W
Zablocki, Kyle R
Petersen, Latrisha K
Uhrich, Kathryn E
Author_xml – sequence: 1
  givenname: Daniel R
  surname: Lewis
  fullname: Lewis, Daniel R
  organization: Department of Chemical & Biochemical Engineering, Department of Biomedical Engineering
– sequence: 2
  givenname: Latrisha K
  surname: Petersen
  fullname: Petersen, Latrisha K
  organization: Department of Biomedical Engineering
– sequence: 3
  givenname: Adam W
  surname: York
  fullname: York, Adam W
  organization: Department of Biomedical Engineering
– sequence: 4
  givenname: Kyle R
  surname: Zablocki
  fullname: Zablocki, Kyle R
  organization: Department of Biomedical Engineering
– sequence: 5
  givenname: Laurie B
  surname: Joseph
  fullname: Joseph, Laurie B
  organization: Department of Pharmacology
– sequence: 6
  givenname: Vladyslav
  surname: Kholodovych
  fullname: Kholodovych, Vladyslav
  organization: Office of Information Technology, Division of High Performance & Research Computing, Rutgers University, Piscataway, NJ 08854; and
– sequence: 7
  givenname: Robert K
  surname: Prud'homme
  fullname: Prud'homme, Robert K
  organization: Department of Chemical & Biomolecular Engineering, Princeton University, Princeton, NJ 08544
– sequence: 8
  givenname: Kathryn E
  surname: Uhrich
  fullname: Uhrich, Kathryn E
  organization: Department of Chemistry and Chemical Biology, and
– sequence: 9
  givenname: Prabhas V
  surname: Moghe
  fullname: Moghe, Prabhas V
  email: moghe@rutgers.edu
  organization: Department of Chemical & Biochemical Engineering, Department of Biomedical Engineering, moghe@rutgers.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25691739$$D View this record in MEDLINE/PubMed
BookMark eNpNUE1LxDAUDLLi7lbP3qRHL11f0jRpjrJ-woIH9Vxe08SNtGlN2gX_vQVXEIY3wzA85r01WfjeG0IuKWwoyPxm8Bg3lDNeKE4pOyErCopmgitY_NNLso7xEwBUUcIZWbJCKCpztSJ3r9MHhqzGaJoUu2HvZrROpx59P2AYnW5NTDEEE8cUx70JfZytebqYOp8e3KE_J6cW22gujpyQ94f7t-1Ttnt5fN7e7jLNhRgzakHlUgtZY07zumHKFBKs1bqG2YPc6ILrklFmQRRSay4ZYmkRlVaWWZaQ69-9Q-i_prlQ1bmoTduiN_0UKyoEKCbl_JCEXB2jU92ZphqC6zB8V3-Xsx_CeV4o
CitedBy_id crossref_primary_10_1016_j_jddst_2024_106334
crossref_primary_10_1186_s40035_023_00393_7
crossref_primary_10_1016_j_mattod_2017_05_006
crossref_primary_10_3390_life13040951
crossref_primary_10_3389_fimmu_2017_00923
crossref_primary_10_1002_advs_202104264
crossref_primary_10_1016_j_ijpharm_2023_123737
crossref_primary_10_1016_j_nano_2021_102387
crossref_primary_10_1016_j_biomaterials_2017_07_035
crossref_primary_10_1038_nnano_2017_167
crossref_primary_10_1016_j_snb_2024_137182
crossref_primary_10_1002_adhm_201500126
crossref_primary_10_1161_ATVBAHA_118_311569
crossref_primary_10_1002_advs_201800781
crossref_primary_10_1016_j_ejpb_2021_05_027
crossref_primary_10_1016_j_pharmthera_2020_107521
crossref_primary_10_1186_s12951_022_01279_y
crossref_primary_10_1016_j_actbio_2023_09_011
crossref_primary_10_1016_j_jconrel_2016_05_049
crossref_primary_10_1038_s41427_024_00548_6
crossref_primary_10_1126_scitranslmed_aay1063
crossref_primary_10_1186_s40580_021_00270_x
crossref_primary_10_1073_pnas_2201443119
crossref_primary_10_1002_ppsc_202000311
crossref_primary_10_1016_j_biomaterials_2016_10_001
crossref_primary_10_1016_j_ijpharm_2019_01_023
crossref_primary_10_1002_adfm_202421512
crossref_primary_10_3390_pharmaceutics12111056
crossref_primary_10_1002_smll_202200967
crossref_primary_10_1038_s41392_019_0068_3
crossref_primary_10_1016_j_atherosclerosis_2019_09_023
crossref_primary_10_1016_j_biomaterials_2021_120875
crossref_primary_10_1016_j_actbio_2017_05_029
crossref_primary_10_1038_srep22910
crossref_primary_10_3390_cells12040522
crossref_primary_10_1002_adma_201902604
crossref_primary_10_1080_14728222_2023_2288272
crossref_primary_10_1016_j_addr_2017_08_003
crossref_primary_10_1039_D4NR00252K
crossref_primary_10_3390_ijms23052522
crossref_primary_10_1002_advs_202504990
crossref_primary_10_1093_cvr_cvv271
crossref_primary_10_1016_j_cclet_2022_06_008
crossref_primary_10_1074_jbc_M116_739243
crossref_primary_10_3389_fphar_2021_755569
crossref_primary_10_1002_wnan_1840
crossref_primary_10_1016_j_jstrokecerebrovasdis_2019_03_045
crossref_primary_10_1016_j_nano_2015_09_005
crossref_primary_10_3389_fbioe_2020_00112
crossref_primary_10_1093_cvr_cvae099
crossref_primary_10_1002_adtp_201900208
crossref_primary_10_1007_s40139_019_00196_4
crossref_primary_10_3390_pharmaceutics16081037
crossref_primary_10_3390_app14051939
crossref_primary_10_1002_smll_201601425
crossref_primary_10_1002_smll_202003253
crossref_primary_10_1002_smll_201702793
crossref_primary_10_1016_j_addr_2021_01_005
crossref_primary_10_1016_j_jconrel_2016_12_032
crossref_primary_10_3389_fbioe_2021_686684
crossref_primary_10_1002_anie_202305576
crossref_primary_10_1161_CIRCRESAHA_115_306256
crossref_primary_10_3390_nano8020084
crossref_primary_10_1016_j_biomaterials_2015_12_033
crossref_primary_10_3390_jfb6020171
crossref_primary_10_3390_cryst11101172
crossref_primary_10_1080_10717544_2021_1886199
crossref_primary_10_1007_s11095_017_2211_6
crossref_primary_10_1155_2020_8131754
crossref_primary_10_1007_s11095_016_2000_7
crossref_primary_10_1016_j_atherosclerosis_2019_04_223
crossref_primary_10_1016_j_addr_2018_07_008
crossref_primary_10_1016_j_apmt_2022_101466
crossref_primary_10_1016_j_addr_2024_115204
crossref_primary_10_1038_s41569_021_00629_x
crossref_primary_10_1038_s41569_018_0073_1
crossref_primary_10_1093_cvr_cvv237
crossref_primary_10_1002_adma_201904607
crossref_primary_10_1002_ange_202305576
ContentType Journal Article
DBID CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.1073/pnas.1424594112
DatabaseName Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList MEDLINE
MEDLINE - Academic
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 no_fulltext_linktorsrc
Discipline Sciences (General)
EISSN 1091-6490
ExternalDocumentID 25691739
Genre Research Support, Non-U.S. Gov't
Journal Article
Research Support, N.I.H., Extramural
GrantInformation_xml – fundername: NHLBI NIH HHS
  grantid: R21 HL093753
– fundername: NIBIB NIH HHS
  grantid: EB005583
– fundername: NIBIB NIH HHS
  grantid: T32 EB005583
– fundername: NIGMS NIH HHS
  grantid: T32 GM008339
– fundername: NHLBI NIH HHS
  grantid: R21HL93753
– fundername: NIGMS NIH HHS
  grantid: T32GM008339
– fundername: NIAMS NIH HHS
  grantid: U54AR055073
– fundername: NHLBI NIH HHS
  grantid: R01 HL107913
– fundername: NIAMS NIH HHS
  grantid: U54 AR055073
– fundername: NHLBI NIH HHS
  grantid: R01HL107913
GroupedDBID ---
-DZ
-~X
.55
0R~
123
29P
2AX
2FS
2WC
4.4
53G
5RE
5VS
85S
AACGO
AAFWJ
AANCE
ABBHK
ABOCM
ABPLY
ABPPZ
ABTLG
ABXSQ
ABZEH
ACGOD
ACHIC
ACIWK
ACNCT
ACPRK
ADQXQ
ADULT
AENEX
AEUPB
AEXZC
AFFNX
AFOSN
AFRAH
ALMA_UNASSIGNED_HOLDINGS
AQVQM
BKOMP
CGR
CS3
CUY
CVF
D0L
DCCCD
DIK
DU5
E3Z
EBS
ECM
EIF
EJD
F5P
FRP
GX1
H13
HH5
HYE
IPSME
JAAYA
JBMMH
JENOY
JHFFW
JKQEH
JLS
JLXEF
JPM
JSG
JST
KQ8
L7B
LU7
N9A
NPM
N~3
O9-
OK1
PNE
PQQKQ
R.V
RHI
RNA
RNS
RPM
RXW
SA0
SJN
TAE
TN5
UKR
W8F
WH7
WOQ
WOW
X7M
XSW
Y6R
YBH
YKV
YSK
ZCA
~02
~KM
7X8
ID FETCH-LOGICAL-c466t-1f0937c67ba313bd29e570ffccb07ba03ec54c8212f0657cc472aa8faa9c9f2f2
IEDL.DBID 7X8
ISICitedReferencesCount 100
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000350224900038&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1091-6490
IngestDate Thu Sep 04 19:23:20 EDT 2025
Mon Jul 21 05:58:48 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 9
Keywords atherosclerosis
nanomedicine
macrophages
biomaterials
Language English
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c466t-1f0937c67ba313bd29e570ffccb07ba03ec54c8212f0657cc472aa8faa9c9f2f2
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
OpenAccessLink https://www.pnas.org/content/pnas/112/9/2693.full.pdf
PMID 25691739
PQID 1660927714
PQPubID 23479
ParticipantIDs proquest_miscellaneous_1660927714
pubmed_primary_25691739
PublicationCentury 2000
PublicationDate 2015-03-03
PublicationDateYYYYMMDD 2015-03-03
PublicationDate_xml – month: 03
  year: 2015
  text: 2015-03-03
  day: 03
PublicationDecade 2010
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle Proceedings of the National Academy of Sciences - PNAS
PublicationTitleAlternate Proc Natl Acad Sci U S A
PublicationYear 2015
References 16214597 - Lancet. 2005 Oct 8;366(9493):1267-78
18046703 - Magn Reson Med. 2007 Dec;58(6):1164-70
22223224 - Adv Mater. 2012 Feb 7;24(6):733-9
22835678 - Acta Biomater. 2012 Nov;8(11):3956-62
19405544 - Biomacromolecules. 2009 Jun 8;10(6):1381-91
17531655 - J Am Coll Cardiol. 2007 May 29;49(21):2073-80
19487682 - Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9815-9
24972372 - Mol Pharm. 2014 Aug 4;11(8):2815-24
15031495 - Science. 2004 Mar 19;303(5665):1813-8
23891521 - Biomaterials. 2013 Oct;34(32):7950-9
21816466 - Biomaterials. 2011 Nov;32(32):8319-27
2251254 - Proc Natl Acad Sci U S A. 1990 Dec;87(23):9133-7
21523920 - Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2011 Jul-Aug;3(4):400-20
14980540 - Drug Discov Today. 2004 Mar 1;9(5):219-28
18672949 - Mol Pharm. 2008 Jul-Aug;5(4):505-15
11877368 - Circulation. 2002 Mar 5;105(9):1135-43
20170758 - Acta Biomater. 2010 Aug;6(8):3081-91
16768400 - Biomacromolecules. 2006 Jun;7(6):1796-805
19644120 - Science. 2009 Jul 31;325(5940):612-6
17891134 - Nat Biotechnol. 2007 Oct;25(10):1165-70
23795777 - Biomacromolecules. 2013 Aug 12;14(8):2463-9
9974397 - Arterioscler Thromb Vasc Biol. 1999 Feb;19(2):187-95
23738575 - Biomacromolecules. 2013 Aug 12;14(8):2499-509
8696943 - Arterioscler Thromb Vasc Biol. 1996 Aug;16(8):1033-9
11073835 - Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):2336-45
11229870 - Front Biosci. 2001 Mar 1;6:D515-25
15638783 - Curr Vasc Pharmacol. 2005 Jan;3(1):63-8
22179539 - Circulation. 2012 Jan 3;125(1):e2-e220
8982823 - J Anat. 1996 Dec;189 ( Pt 3):503-5
16452560 - N Engl J Med. 2006 Feb 2;354(5):483-95
12482824 - Arterioscler Thromb Vasc Biol. 2002 Dec 1;22(12):1990-5
17675037 - Atherosclerosis. 2008 Feb;196(2):598-607
References_xml – reference: 16214597 - Lancet. 2005 Oct 8;366(9493):1267-78
– reference: 9974397 - Arterioscler Thromb Vasc Biol. 1999 Feb;19(2):187-95
– reference: 19644120 - Science. 2009 Jul 31;325(5940):612-6
– reference: 8696943 - Arterioscler Thromb Vasc Biol. 1996 Aug;16(8):1033-9
– reference: 17675037 - Atherosclerosis. 2008 Feb;196(2):598-607
– reference: 20170758 - Acta Biomater. 2010 Aug;6(8):3081-91
– reference: 22835678 - Acta Biomater. 2012 Nov;8(11):3956-62
– reference: 21816466 - Biomaterials. 2011 Nov;32(32):8319-27
– reference: 21523920 - Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2011 Jul-Aug;3(4):400-20
– reference: 11229870 - Front Biosci. 2001 Mar 1;6:D515-25
– reference: 2251254 - Proc Natl Acad Sci U S A. 1990 Dec;87(23):9133-7
– reference: 19487682 - Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9815-9
– reference: 8982823 - J Anat. 1996 Dec;189 ( Pt 3):503-5
– reference: 19405544 - Biomacromolecules. 2009 Jun 8;10(6):1381-91
– reference: 23891521 - Biomaterials. 2013 Oct;34(32):7950-9
– reference: 14980540 - Drug Discov Today. 2004 Mar 1;9(5):219-28
– reference: 17891134 - Nat Biotechnol. 2007 Oct;25(10):1165-70
– reference: 11073835 - Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):2336-45
– reference: 17531655 - J Am Coll Cardiol. 2007 May 29;49(21):2073-80
– reference: 16452560 - N Engl J Med. 2006 Feb 2;354(5):483-95
– reference: 11877368 - Circulation. 2002 Mar 5;105(9):1135-43
– reference: 15638783 - Curr Vasc Pharmacol. 2005 Jan;3(1):63-8
– reference: 24972372 - Mol Pharm. 2014 Aug 4;11(8):2815-24
– reference: 18046703 - Magn Reson Med. 2007 Dec;58(6):1164-70
– reference: 22179539 - Circulation. 2012 Jan 3;125(1):e2-e220
– reference: 16768400 - Biomacromolecules. 2006 Jun;7(6):1796-805
– reference: 22223224 - Adv Mater. 2012 Feb 7;24(6):733-9
– reference: 23738575 - Biomacromolecules. 2013 Aug 12;14(8):2499-509
– reference: 23795777 - Biomacromolecules. 2013 Aug 12;14(8):2463-9
– reference: 18672949 - Mol Pharm. 2008 Jul-Aug;5(4):505-15
– reference: 12482824 - Arterioscler Thromb Vasc Biol. 2002 Dec 1;22(12):1990-5
– reference: 15031495 - Science. 2004 Mar 19;303(5665):1813-8
SSID ssj0009580
Score 2.4868255
Snippet Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a focal trigger of chronic coronary, intracranial, and peripheral arterial...
SourceID proquest
pubmed
SourceType Aggregation Database
Index Database
StartPage 2693
SubjectTerms Animals
Atherosclerosis - drug therapy
Atherosclerosis - genetics
Atherosclerosis - metabolism
Atherosclerosis - pathology
Carbohydrates
CD36 Antigens - genetics
CD36 Antigens - metabolism
Humans
Hyperplasia - genetics
Hyperplasia - metabolism
Hyperplasia - pathology
Lipids
Macrophages - metabolism
Macrophages - pathology
Mice
Mice, Knockout
Nanoparticles
Neointima - genetics
Neointima - metabolism
Neointima - pathology
Oxidation-Reduction
Plaque, Atherosclerotic - blood
Plaque, Atherosclerotic - drug therapy
Plaque, Atherosclerotic - genetics
Plaque, Atherosclerotic - metabolism
Plaque, Atherosclerotic - pathology
Scavenger Receptors, Class A - genetics
Scavenger Receptors, Class A - metabolism
Title Sugar-based amphiphilic nanoparticles arrest atherosclerosis in vivo
URI https://www.ncbi.nlm.nih.gov/pubmed/25691739
https://www.proquest.com/docview/1660927714
Volume 112
WOSCitedRecordID wos000350224900038&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText
inHoldings 1
isFullTextHit
isPrint
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV07T8MwELaAMrAA5VleMhIDDKZ5OHY8IQRULFSVAKlbdHFslCUJTdvfzzlJBQsSEosHS5Gi8_m-z-fzfYRcRUj5EQaBBVJrxq0xLEWcYzYyJjaI2AagEZuQ43E8napJl3Cru7LKVUxsAnVWapcjH_pCeCqQ0ud31SdzqlHudrWT0FgnvRCpjPNqOY1_NN2N224EymeCK2_V2keGw6qA-ta98ooU950c5W_8ssGZ0c5__3CXbHcMk963LtEna6bYI_1uD9f0ums0fbNPHl8XHzBjDsgyCriseeXSK5oWUOBZuiuZo9Dod9CGKpY1TuGY1zQv6DJflgfkffT09vDMOlUFprkQc-ZbDymJFjIFtFmaBcpE0rNW69TDOS80OuI6RkizSE9wBbkMAGILoLSygQ0OyUZRFuaYUOlryARGS2R9HIyNTcBBqYwLbtNUhQNyubJUgl7rriKgMOWiTr5tNSBHrbmTqm2vkSAJwzNkqE7-8PUp2UIGEzVFYeEZ6Vncs-acbOrlPK9nF4074DievHwBrXrA_A
linkProvider ProQuest
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=Sugar-based+amphiphilic+nanoparticles+arrest+atherosclerosis+in+vivo&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+-+PNAS&rft.au=Lewis%2C+Daniel+R&rft.au=Petersen%2C+Latrisha+K&rft.au=York%2C+Adam+W&rft.au=Zablocki%2C+Kyle+R&rft.date=2015-03-03&rft.eissn=1091-6490&rft.volume=112&rft.issue=9&rft.spage=2693&rft_id=info:doi/10.1073%2Fpnas.1424594112&rft_id=info%3Apmid%2F25691739&rft_id=info%3Apmid%2F25691739&rft.externalDocID=25691739
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1091-6490&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1091-6490&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1091-6490&client=summon