Duchenne Muscular Dystrophy: Mechanisms and Therapeutic Strategies
A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".
Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 33353
Special Issue Editor
Interests: SR calcium handling in heart and skeletal muscles; muscle differentiation; mitochondrial calcium; Duchenne muscular dystrophy; myocardial infarction; heart failure; AAV mediated gene therapy
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Duchenne muscular dystrophy (DMD) is one of the most prevalent forms of muscular dystrophy. DMD is an X-linked recessive disorder, epidemiologically reported to affect 1 in 3600–6000 male live births. DMD is caused by mutations in the dystrophin gene resulting in a loss of functional dystrophin protein in skeletal and cardiac muscles. This leads to the degeneration of muscle fibers, necrosis, inflammation, fibrosis, and fatty replacement resulting in muscle weakness, respiratory and cardiac failure, and premature death. Despite these findings and several clinical trials, there is no curative treatment for this disease. Although the loss of dystrophin is the primary cause, several cellular and molecular factors including calcium handling proteins, myogenic factors, proteases, signaling molecules, and altered expressions of genes have been identified as key players in muscle pathogenesis and the development of dystrophic cardiomyopathy. This Special Issue will provide a general overview of cellular and molecular mechanisms associated with muscle wasting and the development of dystrophic cardiomyopathy and therapeutic strategies in treating DMD.
We look forward to your contributions of original research or review articles that fit the theme of this Special Issue.
Dr. Gopal J. Babu
Guest Editor
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Keywords
- Duchenne muscular dystrophy
- dystrophin
- Calcium
- gene therapy
- muscle wasting
- cardiomyopathy
- muscle regeneration
- metabolic dysfunction
- proteases
- inflammation
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