Mitochondrial dysfunction and vascular aging in comorbid pathology

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