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Molecular and cell biology of skeletal muscle regeneration

  • Chapter
Molecular and Cell Biology of Muscular Dystrophy

Part of the book series: Molecular and Cell Biology of Human Diseases Series ((Mol. Cell Biol. Hu. Dis.))

Abstract

When skeletal muscle is damaged, it is repaired by the proliferation of mononuclear muscle precursor cells (mpc) which fuse either with one another to form young multinucleated muscle cells (myotubes) or with the ends of damaged myofibres (Robertson et al., 1990). The success of new muscle formation is related to the size of the injury, as after major trauma and extensive disruption of the external lamina of muscle fibres there is often significant replacement by fibrous and cellular connective tissue. Impaired muscle regeneration and progressive replacement by fat and connective tissue is a feature of myopathies such as Duchenne muscular dystrophy (DMD), although this results from many small discrete lesions constantly recurring over a long period of time rather than from a single large injury. Failed regeneration can be seen in simplistic terms as a failure of muscle precursor replication. In this review we shall concentrate on the biology of muscle precursor cells. For coverage of other aspects of regeneration such as resealing of damaged myofibres, revascularization and reinnervation, see Grounds (1991).

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Authors
  1. Miranda D. Grounds
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  2. Zipora Yablonka-Reuveni
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Editors and Affiliations

  1. Charing Cross & Westminster Medical School, University of London, UK

    Terence Partridge

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© 1993 Springer Science+Business Media Dordrecht

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Grounds, M.D., Yablonka-Reuveni, Z. (1993). Molecular and cell biology of skeletal muscle regeneration. In: Partridge, T. (eds) Molecular and Cell Biology of Muscular Dystrophy. Molecular and Cell Biology of Human Diseases Series. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1528-5_9

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  • DOI: https://doi.org/10.1007/978-94-011-1528-5_9

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-4667-1

  • Online ISBN: 978-94-011-1528-5

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