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Vascular Aging and Oxidative Stress: Hormesis and Adaptive Cellular Pathways

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Aging and Age-Related Disorders

Abstract

The biochemical basis of aging in general and of vascular aging in particular is the progressive failure of maintenance and repair systems due to cumulative molecular damage. One of the major sources of damage is reactive oxygen species (ROS). Indeed, all organisms living in an aerobic environment are exposed to ROS on a continual basis, generated as by-products of normal cellular metabolism and taken up from the external environment. In fact, oxidative damage is widely used as a biomarker of aging and diseases. At the cellular level, molecular damage and oxidative stress lead to cellular senescence. Endothelial senescent cells are proinflammatory, proatherosclerotic, and prothrombotic and could participate in the process of aging and atherosclerosis. ROS, however, also play a crucial role in physiologic cell function when present at a low physiologic concentration. Therefore, we believe that the exposure of the endothelium to physiologic oxidative stress during its maturation phase determines vascular longevity. This process is known as hormesis: mild stress activates different endogenous mechanisms of repair and maintenance to protect cells against subsequent stresses. In the case of endothelial cells, exposure to mild oxidative stress during the maturation phase of the endothelium will activate protective pathways involved in stress resistance. It is the cumulative and chronic stress that induce progressive failure of protective mechanisms, leading to higher susceptibility to diseases, cellular senescence, aging, and ultimately death.

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Thorin-Trescases, N., Thorin, E. (2010). Vascular Aging and Oxidative Stress: Hormesis and Adaptive Cellular Pathways. In: Bondy, S., Maiese, K. (eds) Aging and Age-Related Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-602-3_15

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