Calcium handling dysfunction and cardiac damage following acute ventricular preload challenge in the dystrophin-deficient mouse heart

Author:

Haffner Vivian1,Nourian Zahra1,Boerman Erika M.1ORCID,Lambert Michelle D.1,Hanft Laurin M.1,Krenz Maike12,Baines Christopher P.32,Duan Dongsheng45,McDonald Kerry S.1ORCID,Domeier Timothy L.16ORCID

Affiliation:

1. Department of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, Missouri, United States

2. The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States

3. Department of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, Missouri, United States

4. Department of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, Missouri, United States

5. Department of Neurology, School of Medicine, University of Missouri, Columbia, Missouri, United States

6. Department of Medicine, School of Medicine, University of Missouri, Columbia, Missouri, United States

Abstract

The mechanisms of cardiac disease progression in muscular dystrophy are complex and poorly understood. Using a transgenic mouse model with cardiomyocyte-specific expression of the GCaMP6f Ca2+ indicator, the present study provides further support for the Ca2+-overload hypothesis of disease progression and ventricular arrhythmogenesis in muscular dystrophy.

Funder

University of Missouri System

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases

U.S. Department of Defense

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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