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Review
. 2010 Mar;19(2):201-7.
doi: 10.1097/MNH.0b013e3283361c0b.

Arterial aging: a journey into subclinical arterial disease

Mingyi Wang  1 , Robert E Monticone, Edward G Lakatta
Affiliations
Review

Arterial aging: a journey into subclinical arterial disease

Mingyi Wang et al. Curr Opin Nephrol Hypertens. 2010 Mar.

Abstract

Purpose of review: Age-associated arterial alterations in cells, matrix, and biomolecules are the foundation for the initiation and progression of cardiovascular diseases in older persons. This review focuses on the latest advances on the intertwining of aging and disease within the arterial wall at the cell and molecular levels.

Recent findings: Endothelial dysfunction, vascular smooth muscle cell (VSMC) proliferation/invasion/secretion, matrix fragmentation, collagenization and glycation are characteristics of an age-associated arterial phenotype that creates a microenvironment enriched with reactive oxygen species (ROS) for the pathogenesis of arterial disease. This niche creates an age-associated arterial secretory phenotype (AAASP), which is orchestrated by the concerted effects of numerous age-modified angiotensin II signaling molecules. Most of these biomolecular, cell, and matrix modifications that constitute the AAASP can be elicited by experimental hypertension or atherosclerosis at a younger age. The arterial AAASP also shares features of a senescence-associated secretory phenotype (SASP) identified in other mesenchymocytes, that is, fibroblasts.

Summary: A subclinical AAASP evolves during aging. Targeting this subclinical AAASP may reduce the incidence and progression of the quintessential age-associated arterial diseases, that is, hypertension and atherosclerosis.

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Conflict of interest statement

Conflicts of interest

None

Figures

Figure 1
Figure 1
Illustration of potential molecular and cellular mechanisms for arterial proinflammation in the aging-to-disease journey.
See this image and copyright information in PMC

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