Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
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.

PubMed Disclaimer

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

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Aging-dynamics of cancer. at http://www.cdc.gov/nchs/
    1. Humes K. The population 65 years and older: Aging in America. The book of the States. 2005:464–470.
    1. Lakatta EG, Wang M, Najjar SS. Arterial aging and subclinical arterial disease are fundamentally intertwined at macroscopic and molecular levels. Med Clin North Am. 2009;93:583–604. This is a comprehensive overview on the current knowledge on the intertwining of arterial aging and disease. - PMC - PubMed
    1. Lakatta EG. Central arterial aging and the epidemic of systolic hypertension and atherosclerosis. J Am Soc Hypertens. 2007;1:302–340. - PubMed
    1. Wang M, Lakatta EG. The salted artery and angiotensin II signaling: A deadly duo in arterial disease. J Hypertens. 2009;27:19–21. This editorial commentary provides a brief introduction to high salt diets, ang II signaling, aging, and arterial disease. - PMC - PubMed

Publication types