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Anthracycline-Induced Cardiomyopathy is Manifested in Decreased Protein Synthesis, Impaired Intracellular Regeneration, and Non-Necrotic Death of Cardiomyocytes

Anthracycline-Induced Cardiomyopathy is Manifested in Decreased Protein Synthesis, Impaired... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Bulletin of Experimental Biology and Medicine Springer Journals

Anthracycline-Induced Cardiomyopathy is Manifested in Decreased Protein Synthesis, Impaired Intracellular Regeneration, and Non-Necrotic Death of Cardiomyocytes

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References (9)

Publisher
Springer Journals
Copyright
Copyright © 2001 by Plenum Publishing Corporation
Subject
Biomedicine; Biomedicine, general; Internal Medicine; Cell Biology; Pathology; Laboratory Medicine
ISSN
0007-4888
eISSN
1573-8221
DOI
10.1023/A:1017956922385
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

Bulletin of Experimental Biology and Medicine – Springer Journals

Published: Oct 19, 2004

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