Anthracycline-induced cardiomyopathy is manifested in decreased protein synthesis, impaired intracellular regeneration, and non-necrotic death of cardiomyocytes.
The cytostatic anthracycline antibiotic daunomycin hydrochloride led to the development of plastic myocardial insufficiency characterized by impaired intracellular regeneration of cardiomyocytes and progressive involution of cytoplasmic structures. Morphological signs of plastic myocardial insufficiency included fragmentation, annulation, or collapse of nucleoli in cardiomyocyte nuclei, lysis of myofilaments, sarcomeres, or myofibrils, focal degradation of the cytoplasm, and intensive autophagy. Fatal anthracycline-induced cardiac insufficiency was associated with massive cardiomyocyte loss due to their non-necrotic death and elimination. Our findings indicate that anthracycline-induced cardiomyopathy in laboratory animals is a convenient model for studying general mechanisms underlying the pathogenesis of regenerative and plastic cardiac insufficiency in humans.
Semenov
D E
DE
Department of General Pathology and Pathomorphology, Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. pathol@cyber.nsk.ma.ru
Lushnikova
E L
EL
Nepomnyashchikh
L M
LM
D000818:Animals; D018943:Anthracyclines / Q000494:pharmacology*; D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D017209:Apoptosis; D009202:Cardiomyopathies / Q000139:chemically induced / Q000473:pathology*; D016923:Cell Death; D002466:Cell Nucleolus / Q000187:drug effects; D003593:Cytoplasm / Q000378:metabolism; D003630:Daunorubicin / Q000494:pharmacology; D006321:Heart / Q000187:drug effects*; D008297:Male; D009206:Myocardium / Q000166:cytology* / Q000473:pathology* / Q000648:ultrastructure; D009210:Myofibrils / Q000187:drug effects; D009336:Necrosis; D051381:Rats; D017208:Rats, Wistar; D012518:Sarcomeres / Q000187:drug effects
D018943:Anthracyclines; D000903:Antibiotics, Antineoplastic; D003630:Daunorubicin