Mitochondrial dysfunction and vascular aging in comorbid pathology

Abstract

Cardiovascular diseases take a leading position in the structure of mortality in modern society. Most diseases are characterized by uncontrolled processes of oxidative stress, proteolysis, tissue and cellular hypoxia, which cause endothelial dysfunction. Tissue and cellular hypoxia accumulated with mitochondrial reactive forms of oxygen damaging lipoproteins, proteins, nucleic acids plays an important role in the pathogenesis of vascular aging. Cellular aging is characterized by a decrease in the number of mitochondria, a decrease in the number of copies of mitochondrial DNA, and the loss of mitochondrial protein. In addition to morphological changes, the function of mitochondria is oppressed, at the same time the activity of their proteins and enzymes decreases. Changes in the functions of mitochondria can be secondary in response to various stimuli and are associated with a violation of their structure and a change in activity in response to specific genetic and phenotypic conditions. Reprogramming of mitochondrial biogenesis occupies a central position in the theory of cellular aging and is one of the targets for interventions in prolonging active longevity.