Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Feb 6;13(2):dmm042192.
doi: 10.1242/dmm.042192.

Skeletal muscle in health and disease

Jennifer Morgan  1   2 , Terence Partridge  3   2   4
Affiliations
Review

Skeletal muscle in health and disease

Jennifer Morgan et al. Dis Model Mech. .

Abstract

Skeletal muscle fibres are multinucleated cells that contain postmitotic nuclei (i.e. they are no longer able to divide) and perform muscle contraction. They are formed by fusion of muscle precursor cells, and grow into elongating myofibres by the addition of further precursor cells, called satellite cells, which are also responsible for regeneration following injury. Skeletal muscle regeneration occurs in most muscular dystrophies in response to necrosis of muscle fibres. However, the complex environment within dystrophic skeletal muscle, which includes inflammatory cells, fibroblasts and fibro-adipogenic cells, together with the genetic background of the in vivo model and the muscle being studied, complicates the interpretation of laboratory studies on muscular dystrophies. Many genes are expressed in satellite cells and in other tissues, which makes it difficult to determine the molecular cause of various types of muscular dystrophies. Here, and in the accompanying poster, we discuss our current knowledge of the cellular mechanisms that govern the growth and regeneration of skeletal muscle, and highlight the defects in satellite cell function that give rise to muscular dystrophies.

Keywords: Muscular dystrophy; Satellite cell; Skeletal muscle regeneration.

PubMed Disclaimer

Conflict of interest statement

Competing interestsThe authors declare no competing or financial interests.

References

    1. Abou-Khalil R., Mounier R. and Chazaud B. (2010). Regulation of myogenic stem cell behavior by vessel cells: the “menage a trois” of satellite cells, periendothelial cells and endothelial cells. Cell Cycle 9, 892-896. 10.4161/cc.9.5.10851 - DOI - PubMed
    1. Abu-Baker A., Kharma N., Perreault J., Grant A., Shekarabi M., Maios C., Dona M., Neri C., Dion P. A., Parker A. et al. (2019). RNA-based therapy utilizing oculopharyngeal muscular dystrophy transcript knockdown and replacement. Mol. Ther. Nucleic Acids 15, 12-25. 10.1016/j.omtn.2019.02.003 - DOI - PMC - PubMed
    1. Aguti S., Malerba A. and Zhou H. (2018). The progress of AAV-mediated gene therapy in neuromuscular disorders. Expert Opin Biol. Ther. 18, 681-693. 10.1080/14712598.2018.1479739 - DOI - PubMed
    1. Almeida C. F., Martins P. C. and Vainzof M. (2016). Comparative transcriptome analysis of muscular dystrophy models Large(myd), Dmd(mdx)/Large(myd) and Dmd(mdx): what makes them different? Eur. J. Hum. Genet. 24, 1301-1309. 10.1038/ejhg.2016.16 - DOI - PMC - PubMed
    1. Amthor H., Otto A., Vulin A., Rochat A., Dumonceaux J., Garcia L., Mouisel E., Hourde C., Macharia R., Friedrichs M. et al. (2009). Muscle hypertrophy driven by myostatin blockade does not require stem/precursor-cell activity. Proc. Natl. Acad. Sci. USA 106, 7479-7484. 10.1073/pnas.0811129106 - DOI - PMC - PubMed

Publication types