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Updated: Aug 16, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

Morphological manifestations of heart remodeling in anthracycline-induced dilated cardiomyopathy

E L Lushnikova1, M G Klinnikova, O P Molodykh

  • 1Department of Cell Biology and Morphology, Institute of Regional Pathology and Pathomorphology, Siberian Division, Russian Academy of Medical Sciences, Novosibirsk. pathol@soramn.ru

Bulletin of Experimental Biology and Medicine
|September 2, 2005
PubMed

Insights

Doxorubicin treatment causes dilated cardiomyopathy by reducing heart muscle cell numbers and regeneration. Remaining cells enlarge, and connective tissue stiffens as a compensatory response to heart failure.

Area of Science:

  • Cardiology
  • Toxicology
  • Pathology

Background:

  • Anthracyclines, like doxorubicin, are potent chemotherapy agents.
  • Cardiotoxicity is a significant dose-limiting side effect of anthracycline therapy.
  • Dilated cardiomyopathy is a severe form of heart muscle disease.

Purpose of the Study:

  • To investigate the mechanisms of anthracycline-induced dilated cardiomyopathy.
  • To understand the cardiac remodeling processes following doxorubicin exposure.
  • To elucidate the role of cardiomyocyte loss and regeneration in heart failure.

Main Methods:

  • Administration of a single sublethal dose of doxorubicin to a study model.
  • Analysis of cardiomyocyte depopulation and regenerative capacity.
  • Assessment of myocardial hypertrophy and fibrosis.

Main Results:

  • Doxorubicin treatment led to significant cardiomyocyte depopulation (up to 27%).
  • Reduced regenerative plastic reactions of cardiomyocytes were observed.
  • Hypertrophy of surviving cardiomyocytes and myocardial sclerosis occurred as compensatory responses.

Conclusions:

  • Cardiomyocyte elimination and impaired regeneration are key drivers of doxorubicin-induced heart failure.
  • Heart remodeling is characterized by dilatation and fibrosis.
  • Connective tissue sclerosis represents a compensatory reaction to muscle fiber loss.

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