Related Experiment Video
Updated: Jul 11, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Increased myosin heavy chain-beta with atrial expression of ventricular light chain-2 in canine cardiomyopathy
Geraldine A Fuller1, Sabahattin Bicer, Robert L Hamlin
1Department of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, Columbus, Ohio, USA.
Background:
Dilated cardiomyopathy is a naturally occurring disease in humans and dogs. Human studies have shown increased levels of myosin heavy chain (MHC)-beta in failing ventricles and the left atria (LA) and of ventricular light chain (VLC)-2 in the right atria in dilated cardiomyopathy.
Methods And Results:
This study evaluates the levels of MHC-beta in all heart chambers in prolonged canine right ventricular pacing. In addition, we determined whether levels of VLC2 were altered in these hearts. Failing hearts demonstrated significantly increased levels of MHC-beta in the right atria, right atrial appendage, LA, left atrial appendage (LAA), and right ventricle compared with controls. Significant levels of VLC2 were detected in the right atria of paced hearts. Differences in MHC-beta expression were observed between the LA and the LAA of paced and control dogs. MHC-beta expression was significantly greater in the LA of paced and control dogs compared with their respective LAA.
Conclusions:
The cardiac myosin isoform shifts in this study were similar to those observed in end-stage human heart failure and more severe than those reported in less prolonged pacing models, supporting the use of this model for further study of end-stage human heart failure. The observation of consistent differences between sampling sites, especially LA versus LAA, indicates the need for rigorous sampling consistency in future studies.
Related Concept Videos
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy
Cardiomyopathy I: Introduction and Classification
Heart Failure II: Pathophysiology

