Arterial aging: a journey into subclinical arterial disease.
OBJECTIVE
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.


RESULTS
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.


CONCLUSIONS
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.
Wang
Mingyi
M
Laboratory of Cardiovascular Science, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore 21224, Maryland, USA.
Monticone
Robert E
RE
Lakatta
Edward G
EG
D000375:Aging / Q000502:physiology*; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D001158:Arteries / Q000254:growth & development* / Q000502:physiology*; D050197:Atherosclerosis / Q000473:pathology; D006801:Humans; D015398:Signal Transduction / Q000502:physiology; D014652:Vascular Diseases / Q000473:pathology*
D000804:Angiotensin II