Atherosclerosis and the vascular biology of aging

C. Bilato, M. T. Crow

Research output: Contribution to journalArticle

Abstract

With advancing age, a series of structural, architectural and compositional modifications take place in the vasculature. The diameter of the vessels tends to increase, and thickening of intimal and medial layers is often observed. In the subendothelial space, blood-derived leukocytes and an increased amount of "activated" smooth muscle cells are present. Extracellular matrix accumulates and becomes particularly rich in glycosaminoglycans. Collagen content increases, while elastin fibers appear progressively disorganized, thinner, and frequently fragmented. These changes in the normal architecture of the vessel wall, that could be referred to as "the vasculopathy of aging", are likely to be the consequence of adaptive mechanisms to maintain normal conditions of flow, mechanical stress and/or wall tension. Although many of these features are similar to the histological findings of the atherosclerotic vessels, atherosclerosis and age-related "vasculopathy" are two distinct phenomena. Nonetheless, several experimental observations in animal models suggest a special link between "the vasculopathy of aging" and atherosclerotic disease, and suggest a particular predisposition of the old vessel to develop the atherosclerotic lesion. Compared to vessels from young animals, older ones show a greater reactivity to mechanical injury and to chronic insults. This may reflect changes in the biology of the vessels that are "intrinsic" to the aging process. Indeed, aging affects the function and responsiveness of the endothelium and vascular smooth muscle cells. Endothelial permeability is increased with age, while ability to produce vasoactive substances declines. Smooth muscle cells from old individuals show a growth advantage over the young ones, and display an increased ability to migrate toward chemoattractants. Moreover, the accumulation of advanced glycation end products (AGEs) occurring with aging can trigger a series of cellular events, such as cellular oxidative stress, expression of leukocyte adhesion molecules, endothelial transmigration of monocytes, and smooth muscle cell chemotaxis, all considered important prelesional events in the atherogenesis process. Taken together, the changes occurring with aging, while unproven to initiate lesion formation per se, are likely to accelerate the development of the atherosclerotic plaque and contribute to increased severity of this disease in the elderly.

Original languageEnglish (US)
Pages (from-to)221-234
Number of pages14
JournalAging clinical and experimental research
Volume8
Issue number4
StatePublished - Aug 1996
Externally publishedYes

Fingerprint

Smooth Muscle Myocytes
Blood Vessels
Atherosclerosis
Aptitude
Tunica Intima
Transendothelial and Transepithelial Migration
Mechanical Stress
Advanced Glycosylation End Products
Elastin
Chemotactic Factors
Cell Adhesion Molecules
Atherosclerotic Plaques
Chemotaxis
Glycosaminoglycans
Vascular Smooth Muscle
Endothelium
Extracellular Matrix
Monocytes
Permeability
Oxidative Stress

Keywords

  • Aging
  • Atherosclerosis
  • Endothelium
  • Smooth muscle cell
  • Vasculature

ASJC Scopus subject areas

  • Geriatrics and Gerontology

Cite this

Atherosclerosis and the vascular biology of aging. / Bilato, C.; Crow, M. T.

In: Aging clinical and experimental research, Vol. 8, No. 4, 08.1996, p. 221-234.

Research output: Contribution to journalArticle

Bilato, C & Crow, MT 1996, 'Atherosclerosis and the vascular biology of aging', Aging clinical and experimental research, vol. 8, no. 4, pp. 221-234.
Bilato, C. ; Crow, M. T. / Atherosclerosis and the vascular biology of aging. In: Aging clinical and experimental research. 1996 ; Vol. 8, No. 4. pp. 221-234.
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