Mitochondrial genome and aging of cardiomyocytes

Abstract

The review presents data on the importance of mitochondrial DNA in aging of cardiomocytes. The mechanisms of accumulation of mutations in mtDNA and reduction of its content, as well as the consequences of these phenomena in cardiomyocytes are described. The similarity of the aging processes of cardiomyocytes and skeletal muscle cells and comparison with the aging processes occurring in mononuclear cells of peripheral blood is indicated. The death of cardiomyocytes and skeletal muscle cells leads to the destruction of mutant forms of mtDNA, as a result of which the content of mutant forms of mtDNA, constantly increasing with age, does not exceed 1-2% of the total number of mtDNA molecules. In addition, the death of cardiomyocytes and myocytes is accompanied by the release of CpG-motive cells mtDNA, which can cause local and general inflammation in old age. It is concluded, that in the treatment of elderly patients it is desirable to take into account the degree of aging ("biological age”) of their myocardial and their presence of chronic myocarditis, for which appropriate diagnostic methods should be developed.