Calcium handling dysfunction and cardiac damage following acute ventricular preload challenge in the dystrophin-deficient mouse heart
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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Nov 01, 2023
- Source ID
- 10.1152/ajpheart.00265.2023
Entities
People
- Christopher P. Baines
- Dongsheng Duan
- Erika M Boerman
- Kerry S. McDonald
- Laurin M. Hanft
- Maike Krenz
- Michelle D. Lambert
- Timothy L. Domeier
- Vivian Haffner
- Zahra Nourian
Organizations
- National Heart, Lung, and Blood Institute
- National Institute of Arthritis and Musculoskeletal and Skin Diseases
- United States Department of Defense
- University of Missouri
- University of Missouri System