Abstract

Regenerative and plastic myocardial insufficiency characterized by impaired intracellular regeneration, progressive involution and apoptosis of cardiomyocytes associated with selective cardiotoxic effect of anthracycline antibiotic rubomycin is accompanied by enhanced proliferative and functional activities of fibroblasts and other stromal cells. Elimination of 30% cardiomyocytes and their atrophy are accompanied by the development of diffuse myocardial sclerosis, which is considered as a compensatory reaction of the connective tissue to the decrease in the weight of muscle fibers. Remodeling of the myocardium during anthracycline-induced cardiomyopathy due to changes in the parenchyma-stroma relationships does not lead to severe deformation of the heart, which is a favorable factor for normalization of myocardial architectonics after initiation of regenerative processes.

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