期刊
CIRCULATION RESEARCH
卷 123, 期 7, 页码 825-848出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.118.312563
关键词
aging; endothelium; inflammation; oxidative stress; telomere
资金
- National Institute of Aging [R01 AG048366, R01 AG050238, R44 AG053131, K02 AG045339]
- National Center for Complementary and Integrative Health [K99 AT010017]
- US Department of Veterans Affairs Biomedical Laboratory Research and Development Service [1I01BX002151]
- US Department of Veterans Affairs Geriatric Research, Education, and Clinical Center
Advancing age promotes cardiovascular disease (CVD), the leading cause of death in the United States and many developed nations. Two major age-related arterial phenotypes, large elastic artery stiffening and endothelial dysfunction, are independent predictors of future CVD diagnosis and likely are responsible for the development of CVD in older adults. Not limited to traditional CVD, these age-related changes in the vasculature also contribute to other age-related diseases that influence mammalian health span and potential life span. This review explores mechanisms that influence age-related large elastic artery stiffening and endothelial dysfunction at the tissue level via inflammation and oxidative stress and at the cellular level via Klotho and energy-sensing pathways (AMPK [AMP-activated protein kinase], SIRT [sirtuins], and mTOR [mammalian target of rapamycin]). We also discuss how long-term calorie restriction-a health span - and life span-extending intervention-can prevent many of these age-related vascular phenotypes through the prevention of deleterious alterations in these mechanisms. Lastly, we discuss emerging novel mechanisms of vascular aging, including senescence and genomic instability within cells of the vasculature. As the population of older adults steadily expands, elucidating the cellular and molecular mechanisms of vascular dysfunction with age is critical to better direct appropriate and measured strategies that use pharmacological and lifestyle interventions to reduce risk of CVD within this population.
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