期刊
JOURNAL OF VASCULAR RESEARCH
卷 55, 期 4, 页码 210-223出版社
KARGER
DOI: 10.1159/000490244
关键词
Aging; Chronic stress; Proinflammation; Arterial remodeling; Arterial stiffening
资金
- National Institute on Aging, National Institutes of Health
Age-associated structural and functional remodeling of the arterial wall produces a productive environment for the initiation and progression of hypertension and atherosclerosis. Chronic aging stress induces low-grade proinflammatory signaling and causes cellular proinflammation in arterial walls, which triggers the structural phenotypic shifts characterized by endothelial dysfunction, diffuse intimal-medial thickening, and arterial stiffening. Microscopically, aged arteries exhibit an increase in arterial cell senescence, proliferation, invasion, matrix deposition, elastin fragmentation, calcification, and amyloidosis. These characteristic cellular and matrix alterations not only develop with aging but can also be induced in young animals under experimental proinflammatory stimulation. Interestingly, these changes can also be attenuated in old animals by reducing low-grade inflammatory signaling. Thus, mitigating age-associated proinflammation and arterial phenotype shifts is a potential approach to retard arterial aging and prevent the epidemic of hypertension and atherosclerosis in the elderly. This is a work of the U.S. Government and is not subject to copyright protection in the USA. Foreign copyrights may apply. Published by S. Karger AG, Basel
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