Journal
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
Volume 19, Issue 2, Pages 201-207Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e3283361c0b
Keywords
angiotensin II; arterial aging; arterial disease
Categories
Funding
- National Institute on Aging, National Institutes of Health
- NATIONAL INSTITUTE ON AGING [ZIAAG000237, ZIAAG000236, ZIAAG000240, ZIAAG000239] Funding Source: NIH RePORTER
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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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