Molecular Advances of Muscular Dystrophy

Dear Colleagues,

Muscular Dystrophies (MDs) are defined as a group of inherited genetic conditions that gradually cause the muscles to weaken, leading to an increasing level of disability. MD is caused by changes (mutations) in the genes responsible for the structure and functioning of a person's muscles. The mutations cause changes in the muscle fibers that interfere with the muscles' ability to function. Over time, this causes increasing disability.

There are about seven types of inherited muscle pathologies such as Duchenne MD, Becker MD, FacioScapulohumeral MD, Limb-Girdle MD, Myotonic Dystrophy, Oculopharyngeal MD and Emery-Dreifuss MD.

New research is looking into ways of repairing the genetic mutations and damaged muscles associated with MD. Current research across muscular dystrophies implicates a role for regulatory mechanisms at the level of both transcriptomic and epigenetic events in the disease phenotype, and suggests that the severity of disease is not solely dictated by events related to the underlying genetic mutation. And MDs have been associated with an increasing number of gene mutations involving structural proteins, signaling molecules and/or leading to aberrant mRNA processing or altered post-translational modifications.

This issue will give recent insights into cellular, genomic and proteomics mechanisms that are primarily and secondarily disrupted in MDs, focusing on omics technologies and signaling mechanisms causing muscle degeneration and regeneration, defects in muscle growth and the repair of skeletal.

The Special Issue entitled “Molecular Advances in Muscular Dystrophy” is now open for submissions, welcoming original manuscripts which aims to and reviews dealing with specific aspects of cell signaling and omics in MDs.

Dr. Mariko Taniguchi-Ikeda
Guest Editor

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