Role of oxidative stress in vascular endothelial cells through aging - A double-edged sword

Abstract

The biochemical basis of aging is the progressive failure of maintenance and repair systems due to cumulative molecular damage. Oxidative damage is widely used as a biomarker of aging and diseases, and the oxidative stress theory of aging proposes that reactive oxygen species (ROS), produced as by-products during normal metabolism, cause cumulative irreversible oxidative damage. At the cellular level, oxidative stress leads to premature senescence, observed both in vitro in cultured cells and in vivo in animals and patients with cardiovascular diseases. Nonetheless, ROS play a crucial role in physiological cell function when present at physiological concentration. This process is known as hormesis: mild, physiological stresses activate different endogenous mechanisms of repair and maintenance to protect cells against subsequent stresses. It is likely, therefore, that it is the ability of the cells to adapt and resist to oxidative damage that determines their lifespan. The impact of oxidative stress, the evidence supporting, or not, the oxidative stress theory of aging, and the role of hormesis are presented in the context of the vascular endothelial aging.