Mechanisms of Vascular Aging
- Circ Res. 2018 Sep 14;123(7):849-867. doi: 10.1161/CIRCRESAHA.118.311378.
- 1. From the Vascular Cognitive Impairment Laboratory, Reynolds Oklahoma Center on Aging (Z.U., S.T., A.C.), University of Oklahoma Health Sciences Center, Oklahoma City.
- 2. Department of Geriatric Medicine, Translational Geroscience Laboratory (Z.U., S.T., A.C.), University of Oklahoma Health Sciences Center, Oklahoma City.
- 3. Department of Medical Physics and Informatics, University of Szeged, Hungary (Z.U., A.C.).
- 4. Department of Pulmonology, Semmelweis University of Medicine, Budapest, Hungary (Z.U.).
- 5. Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City (A.J.D.).
- 6. Veterans Affairs Medical Center-Salt Lake City, Geriatrics Research Education and Clinical Center, UT (A.J.D.).
- 7. Barshop Institute for Longevity and Aging Studies (V.G.), University of Texas Health Science Center at San Antonio.
- 8. Department of Physiology (V.G.), University of Texas Health Science Center at San Antonio.
Aging of the vasculature plays a central role in morbidity and mortality of older people. To develop novel treatments for amelioration of unsuccessful vascular aging and prevention of age-related vascular pathologies, it is essential to understand the cellular and functional changes that occur in the vasculature during aging. In this review, the pathophysiological roles of fundamental cellular and molecular mechanisms of aging, including oxidative stress, mitochondrial dysfunction, impaired resistance to molecular stressors, chronic low-grade inflammation, genomic instability, cellular senescence, epigenetic alterations, loss of protein homeostasis, deregulated nutrient sensing, and stem cell dysfunction in the vascular system are considered in terms of their contribution to the pathogenesis of both microvascular and macrovascular diseases associated with old age. The importance of progeronic and antigeronic circulating factors in relation to development of vascular aging phenotypes are discussed. Finally, future directions and opportunities to develop novel interventions to prevent/delay age-related vascular pathologies by targeting fundamental cellular and molecular aging processes are presented.