Arterial aging and subclinical arterial disease are fundamentally intertwined at macroscopic and molecular levels

The structure and function of arteries change throughout a lifetime. Age is the dominant risk factor for hypertension, coronary heart disease, congestive heart failure, and stroke. The cellular/molecular proinflammatory alterations that underlie arterial aging are novel putative candidates to be tar...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:The Medical clinics of North America Ročník 93; číslo 3; s. 583
Hlavní autori: Lakatta, Edward G, Wang, Mingyi, Najjar, Samer S
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.05.2009
Predmet:
Age Factors
Aged
Aged, 80 and over
Aging
Angiotensin II - metabolism
Animals
Coronary Artery Disease - diagnosis
Coronary Artery Disease - pathology
Coronary Vessels - pathology
Endothelium, Vascular - physiopathology
Female
Humans
Hypertension - complications
Hypertension - pathology
Male
Risk Factors
ISSN:1557-9859, 1557-9859
On-line prístup:Zistit podrobnosti o prístupe
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Abstract The structure and function of arteries change throughout a lifetime. Age is the dominant risk factor for hypertension, coronary heart disease, congestive heart failure, and stroke. The cellular/molecular proinflammatory alterations that underlie arterial aging are novel putative candidates to be targeted by interventions aimed at attenuating arterial aging as a major risk factor for cardiovascular diseases. This review provides a landscape of central arterial aging and age-disease interactions, integrating perspectives that range from humans to molecules, with the goal that future therapies for cardiovascular diseases, such as hypertension, also will target the prevention or amelioration of unsuccessful arterial aging.
AbstractList The structure and function of arteries change throughout a lifetime. Age is the dominant risk factor for hypertension, coronary heart disease, congestive heart failure, and stroke. The cellular/molecular proinflammatory alterations that underlie arterial aging are novel putative candidates to be targeted by interventions aimed at attenuating arterial aging as a major risk factor for cardiovascular diseases. This review provides a landscape of central arterial aging and age-disease interactions, integrating perspectives that range from humans to molecules, with the goal that future therapies for cardiovascular diseases, such as hypertension, also will target the prevention or amelioration of unsuccessful arterial aging.
The structure and function of arteries change throughout a lifetime. Age is the dominant risk factor for hypertension, coronary heart disease, congestive heart failure, and stroke. The cellular/molecular proinflammatory alterations that underlie arterial aging are novel putative candidates to be targeted by interventions aimed at attenuating arterial aging as a major risk factor for cardiovascular diseases. This review provides a landscape of central arterial aging and age-disease interactions, integrating perspectives that range from humans to molecules, with the goal that future therapies for cardiovascular diseases, such as hypertension, also will target the prevention or amelioration of unsuccessful arterial aging.The structure and function of arteries change throughout a lifetime. Age is the dominant risk factor for hypertension, coronary heart disease, congestive heart failure, and stroke. The cellular/molecular proinflammatory alterations that underlie arterial aging are novel putative candidates to be targeted by interventions aimed at attenuating arterial aging as a major risk factor for cardiovascular diseases. This review provides a landscape of central arterial aging and age-disease interactions, integrating perspectives that range from humans to molecules, with the goal that future therapies for cardiovascular diseases, such as hypertension, also will target the prevention or amelioration of unsuccessful arterial aging.
Author Wang, Mingyi
Najjar, Samer S
Lakatta, Edward G
Author_xml – sequence: 1
  givenname: Edward G
  surname: Lakatta
  fullname: Lakatta, Edward G
  email: lakattae@grc.nia.nih.gov
  organization: Laboratory of Cardiovascular Science, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. lakattae@grc.nia.nih.gov
– sequence: 2
  givenname: Mingyi
  surname: Wang
  fullname: Wang, Mingyi
– sequence: 3
  givenname: Samer S
  surname: Najjar
  fullname: Najjar, Samer S
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19427493$$D View this record in MEDLINE/PubMed
BookMark eNpNkEtPwzAQhC1URB_wBzggn7g1-BEn8bGqeEmVuMA52tibypXjtHEC6r8nQCtxmtXMt3OYOZmENiAht5wlnPHsYZc0JkAiGNMJEwljxQWZcaXypS6Unvy7p2Qe444xrkSWXZEp16nIUy1n5LDqeuwceApbF7YUgqVxqIx3wZkf9xxbFxEijgbSeggWGgw9eH-kLoxI_-UCWgo9bcB0bTTt3pnftqb1aAYPHfX4iT5ek8safMSbky7Ix9Pj-_pluXl7fl2vNkujWNovEcFUXOemVlLXua2kNTxlmnEjLYNUYia5rkxmClagxcxmKJnivIa8GL_Egtz_9e679jBg7MvGRYPeQ8B2iGWWCyEUlyN4dwKHqkFb7jvXQHcszyOJb8J7b0Y
CitedBy_id crossref_primary_10_1067_j_cpsurg_2017_01_001
crossref_primary_10_1089_aid_2013_0048
crossref_primary_10_1089_jwh_2018_7441
crossref_primary_10_1186_s12929_019_0559_0
crossref_primary_10_1016_j_actbio_2022_05_039
crossref_primary_10_1161_JAHA_113_000725
crossref_primary_10_1186_s12894_023_01340_4
crossref_primary_10_1007_s10439_011_0287_4
crossref_primary_10_1161_HYPERTENSIONAHA_117_10054
crossref_primary_10_1586_erc_11_140
crossref_primary_10_3389_fcvm_2023_1206156
crossref_primary_10_1038_s41598_018_20763_w
crossref_primary_10_1007_s10237_012_0383_x
crossref_primary_10_1016_j_resp_2013_06_016
crossref_primary_10_1097_01_CCN_0000360669_99971_ec
crossref_primary_10_1016_j_yjmcc_2015_01_021
crossref_primary_10_1097_HJH_0000000000003239
crossref_primary_10_1007_s00380_019_01526_7
crossref_primary_10_1016_j_ihj_2017_08_013
crossref_primary_10_1097_HTR_0000000000000449
crossref_primary_10_1152_japplphysiol_01418_2010
crossref_primary_10_1109_TMI_2021_3123912
crossref_primary_10_1136_bmjopen_2013_004521
crossref_primary_10_1371_journal_pone_0253730
crossref_primary_10_3389_fcvm_2022_899307
crossref_primary_10_1007_s10237_018_1026_7
crossref_primary_10_3390_jcm11123557
crossref_primary_10_1016_j_jcp_2012_09_016
crossref_primary_10_1016_j_piutam_2014_01_033
crossref_primary_10_1111_acel_70108
crossref_primary_10_1016_j_jacc_2012_03_016
crossref_primary_10_1007_s10741_012_9299_x
crossref_primary_10_1016_j_artres_2016_04_001
crossref_primary_10_1111_acel_14197
crossref_primary_10_1152_japplphysiol_01296_2013
crossref_primary_10_1002_prca_201200138
crossref_primary_10_1016_j_jcmg_2015_08_001
crossref_primary_10_1161_HYPERTENSIONAHA_109_148783
crossref_primary_10_1161_HYPERTENSIONAHA_117_10437
crossref_primary_10_1161_HYPERTENSIONAHA_115_06262
crossref_primary_10_1177_1358863X10382946
crossref_primary_10_1002_ehf2_12495
crossref_primary_10_1161_CIRCRESAHA_121_319843
crossref_primary_10_1155_2014_615312
crossref_primary_10_1016_j_ijcard_2011_01_041
crossref_primary_10_1007_s10237_025_01981_4
crossref_primary_10_1016_j_atherosclerosis_2011_08_003
crossref_primary_10_3390_ijms252011188
crossref_primary_10_1016_j_arr_2020_101176
crossref_primary_10_1161_HYPERTENSIONAHA_111_179242
crossref_primary_10_1016_j_hfc_2011_08_011
crossref_primary_10_1161_STROKEAHA_110_583856
crossref_primary_10_1016_j_echo_2014_05_014
crossref_primary_10_1186_s13054_014_0511_3
crossref_primary_10_1111_micc_12487
crossref_primary_10_1007_s10741_010_9161_y
crossref_primary_10_1097_MNH_0b013e3283361c0b
crossref_primary_10_1186_s12986_018_0244_4
crossref_primary_10_2459_JCM_0000000000000229
crossref_primary_10_1113_JP274189
crossref_primary_10_1161_HYPERTENSIONAHA_112_201699
crossref_primary_10_1161_CIRCRESAHA_114_304936
crossref_primary_10_1161_CIRCRESAHA_118_312563
crossref_primary_10_1161_HYPERTENSIONAHA_117_09027
crossref_primary_10_1007_s10237_017_0953_z
crossref_primary_10_1111_jgs_15634
crossref_primary_10_1007_s11906_020_1017_9
crossref_primary_10_1007_s11906_014_0523_z
crossref_primary_10_1136_heartasia_2016_010832
crossref_primary_10_1007_s10741_011_9270_2
crossref_primary_10_1097_CRD_0000000000000911
crossref_primary_10_1038_s41440_018_0181_7
crossref_primary_10_1097_FJC_0000000000000480
crossref_primary_10_1161_HYPERTENSIONAHA_115_05949
crossref_primary_10_1161_HYPERTENSIONAHA_112_196840
crossref_primary_10_1177_1358863X11419996
crossref_primary_10_1007_s00246_016_1373_z
crossref_primary_10_1016_j_artres_2013_01_003
crossref_primary_10_1161_HYPERTENSIONAHA_112_191270
crossref_primary_10_1111_j_1474_9726_2012_00813_x
crossref_primary_10_1016_j_tem_2013_10_002
crossref_primary_10_1093_cvr_cvac007
crossref_primary_10_1155_2012_915057
crossref_primary_10_1136_bmjopen_2016_011031
crossref_primary_10_1136_bmjopen_2016_011891
crossref_primary_10_1097_01_NURSE_0000371063_85604_7c
crossref_primary_10_1016_j_jmbbm_2013_01_026
crossref_primary_10_1161_JAHA_120_018419
crossref_primary_10_1016_j_jvssci_2024_100209
crossref_primary_10_1016_j_semnephrol_2014_08_004
crossref_primary_10_1177_15598276211049320
crossref_primary_10_1007_s11897_013_0163_7
crossref_primary_10_1007_s00421_017_3541_0
crossref_primary_10_1007_s10237_016_0845_7
crossref_primary_10_1097_HJH_0000000000002400
crossref_primary_10_3390_diagnostics12112817
crossref_primary_10_1093_cvr_cvaf137
crossref_primary_10_1210_en_2019_00258
crossref_primary_10_1016_j_vascn_2022_107184
crossref_primary_10_1007_s12170_011_0193_1
crossref_primary_10_1371_journal_pone_0173177
crossref_primary_10_3389_fphar_2020_535395
crossref_primary_10_1016_j_jacc_2011_02_014
crossref_primary_10_1007_s10439_013_0799_1
crossref_primary_10_1007_s40292_019_00318_4
crossref_primary_10_1371_journal_pone_0016653
crossref_primary_10_1038_ajh_2010_192
crossref_primary_10_1016_j_jbiomech_2011_11_021
crossref_primary_10_1002_ehf2_13274
crossref_primary_10_1111_jcpt_12121
crossref_primary_10_1002_acn3_50927
crossref_primary_10_3389_fphys_2021_746796
ContentType Journal Article
DBID CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.1016/j.mcna.2009.02.008
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 Medicine
EISSN 1557-9859
ExternalDocumentID 19427493
Genre Journal Article
Research Support, N.I.H., Intramural
Review
GrantInformation_xml – fundername: Intramural NIH HHS
  grantid: Z01 AG000856
GroupedDBID ---
-ET
-RU
.1-
.55
.FO
.GJ
0R~
1CY
1KJ
1P~
39C
3O-
4.4
457
4CK
53G
5GY
5RE
85S
AAEDT
AAEDW
AAIKC
AALRI
AAMNW
AAQQT
AAQXK
AAWTL
AAXUO
ABCQX
ABDPE
ABFRF
ABJNI
ABMAC
ABPPZ
ABQZK
ABWVN
ACGFO
ACRPL
ADBBV
ADMUD
ADNMO
AEFWE
AENEX
AEVXI
AFCTW
AFFNX
AFRHN
AFTJW
AGQPQ
AJUYK
ALMA_UNASSIGNED_HOLDINGS
AMRAJ
APXCP
ASPBG
AVWKF
AXIYT
AZFZN
B08
CGR
COIAO
CS3
CUY
CVF
DAHGL
DU5
EBS
ECM
EIF
EJD
EX3
F5P
FDB
FEDTE
FGOYB
HVGLF
HZ~
IH2
J5H
L7B
N4W
NPM
O9-
OD.
OHT
OO~
P2P
R2-
SEL
SES
TWZ
UCV
UDS
WH7
WOW
X7M
XOL
YZZ
Z5R
ZE2
ZGI
ZXP
7X8
ID FETCH-LOGICAL-c504t-eeacb197cf539f7db3dc140901c3d0a43e6319bc6c808ede6d6e30511fa787cf2
IEDL.DBID 7X8
ISICitedReferencesCount 148
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000266784000006&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1557-9859
IngestDate Thu Oct 02 11:13:21 EDT 2025
Mon Jul 21 05:30:45 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 3
Language English
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c504t-eeacb197cf539f7db3dc140901c3d0a43e6319bc6c808ede6d6e30511fa787cf2
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
OpenAccessLink http://doi.org/10.1016/j.mcna.2009.02.008
PMID 19427493
PQID 67222513
PQPubID 23479
ParticipantIDs proquest_miscellaneous_67222513
pubmed_primary_19427493
PublicationCentury 2000
PublicationDate 2009-05-01
PublicationDateYYYYMMDD 2009-05-01
PublicationDate_xml – month: 05
  year: 2009
  text: 2009-05-01
  day: 01
PublicationDecade 2000
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle The Medical clinics of North America
PublicationTitleAlternate Med Clin North Am
PublicationYear 2009
SSID ssj0015266
Score 2.3041615
SecondaryResourceType review_article
Snippet The structure and function of arteries change throughout a lifetime. Age is the dominant risk factor for hypertension, coronary heart disease, congestive heart...
SourceID proquest
pubmed
SourceType Aggregation Database
Index Database
StartPage 583
SubjectTerms Age Factors
Aged
Aged, 80 and over
Aging
Angiotensin II - metabolism
Animals
Coronary Artery Disease - diagnosis
Coronary Artery Disease - pathology
Coronary Vessels - pathology
Endothelium, Vascular - physiopathology
Female
Humans
Hypertension - complications
Hypertension - pathology
Male
Risk Factors
Title Arterial aging and subclinical arterial disease are fundamentally intertwined at macroscopic and molecular levels
URI https://www.ncbi.nlm.nih.gov/pubmed/19427493
https://www.proquest.com/docview/67222513
Volume 93
WOSCitedRecordID wos000266784000006&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/eLvHCXMwpV1JSwMxFA7VinhxX-qag9fgpMlMEhCkiMWDLT0o9FayQqGdaZ1W8d-bZGbwJB68zGGWMCRvS77vvQfArUq1UVQoZJwjiHJBkZQiQzpNHOaMMCJjyfwXNhzy8ViMWuC-yYUJtMrGJkZDbQodzsjvMhZ2Jpg8LJYo9IwK2GrdQGMDtIkPZIJMs_EPhpB2I1LpHSZDgqeiTpmp2F1zncu6WmWo2Ml_DzCjo-nv_e8X98FuHWDCXiURB6Bl80OwPagh9COw7AUSp5c6GPsTQZkbWK5VkyEJZfO4hm78DQtdyBep2gDMvuA0Egk-_XAGyhWcy-BqdbGY6jjavOm4C2eBkVQeg7f-0-vjM6r7LoQVoitkvTFWWDDtUiIcM4oYHepiJVgTk0hKbOYVV-lM84RbYzOTWW82MHbSq7923ROwmRe5PQMQE_8WM9xwYilTiTJKG0kTIqX2mx_eATfNVE68XAewQua2WJeTZjI74LRajcmiKr8xwYL6rbQg539-ewF2KvAn8BMvQdt5jbZXYEt_rKbl-3UUF38djgbfFljNsg
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=Arterial+aging+and+subclinical+arterial+disease+are+fundamentally+intertwined+at+macroscopic+and+molecular+levels&rft.jtitle=The+Medical+clinics+of+North+America&rft.au=Lakatta%2C+Edward+G&rft.au=Wang%2C+Mingyi&rft.au=Najjar%2C+Samer+S&rft.date=2009-05-01&rft.eissn=1557-9859&rft.volume=93&rft.issue=3&rft.spage=583&rft_id=info:doi/10.1016%2Fj.mcna.2009.02.008&rft_id=info%3Apmid%2F19427493&rft_id=info%3Apmid%2F19427493&rft.externalDocID=19427493
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1557-9859&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1557-9859&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1557-9859&client=summon