Arterial Aging and Subclinical Arterial Disease are Fundamentally Intertwined at Macroscopic and Molecular Levels

Edward G. Lakatta; Mingyi Wang; Samer S. Najjar

doi:10.1016/j.mcna.2009.02.008

Arterial Aging and Subclinical Arterial Disease are Fundamentally Intertwined at Macroscopic and Molecular Levels

Edward G. Lakatta, Mingyi Wang, Samer S. Najjar

Research output: Contribution to journal › Review article › peer-review

132 Scopus citations

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.

Original language	English (US)
Pages (from-to)	583-604
Number of pages	22
Journal	Medical Clinics of North America
Volume	93
Issue number	3
DOIs	https://doi.org/10.1016/j.mcna.2009.02.008
State	Published - May 2009
Externally published	Yes

Keywords

Angiotensin II
Arterial aging
Arteriosclerosis
Hypertension
Intimal-medial thickening

ASJC Scopus subject areas

General Medicine

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10.1016/j.mcna.2009.02.008

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title = "Arterial Aging and Subclinical Arterial Disease are Fundamentally Intertwined at Macroscopic and Molecular Levels",

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.",

keywords = "Angiotensin II, Arterial aging, Arteriosclerosis, Hypertension, Intimal-medial thickening",

author = "Lakatta, {Edward G.} and Mingyi Wang and Najjar, {Samer S.}",

note = "Funding Information: This research was supported by the Intramural Research Program of the National Institute on Aging, National Institutes of Health. ",

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doi = "10.1016/j.mcna.2009.02.008",

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T1 - Arterial Aging and Subclinical Arterial Disease are Fundamentally Intertwined at Macroscopic and Molecular Levels

AU - Lakatta, Edward G.

AU - Wang, Mingyi

AU - Najjar, Samer S.

N1 - Funding Information: This research was supported by the Intramural Research Program of the National Institute on Aging, National Institutes of Health.

PY - 2009/5

Y1 - 2009/5

N2 - 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.

AB - 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.

KW - Angiotensin II

KW - Arterial aging

KW - Arteriosclerosis

KW - Hypertension

KW - Intimal-medial thickening

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Arterial Aging and Subclinical Arterial Disease are Fundamentally Intertwined at Macroscopic and Molecular Levels

Abstract

Keywords

ASJC Scopus subject areas

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