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Cited by 740Muscle Physiology and DisordersWound Healing and TreatmentsCardiac Fibrosis and Remodeling

Regulation of Muscle Growth and Regeneration by the Immune System

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Tidball, James G.·2017·Nature Reviews Immunology
DOI 10.1038/nri.2016.150PMC PMC5452982
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Abstract

Diseases of muscle that are caused by pathological interactions between muscle and the immune system are devastating, but rare. However, muscle injuries that involve trauma and regeneration are fairly common, and inflammation is a clear feature of the regenerative process. Investigations of the inflammatory response to muscle injury have now revealed that the apparently nonspecific inflammatory response to trauma is actually a complex and coordinated interaction between muscle and the immune system that determines the success or failure of tissue regeneration.

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  • In myocytes, binding of TNF-α to its receptor TNF-R activates the p38-MAPK pathway, leading to silencing of target genes such as Pax7 and Notch1, promoting satellite cell differentiation into myotubes.

    “In myocytes, the binding of TNF-α to its receptor TNF-R activates the p38-mitogen-activated protein kinase (MAPK) pathway, leading to a silencing of target genes such as Pax7 and Notch1 (via an epigenetic control), promoting satellite cell differentiation into myotubes [39]”

    From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [39]

    In “Muscle–myeloid cell interactions during the early, proliferative stage of muscle regeneration” (page unavailable), the review describes TNF signalling through p38α repressing PAX7 via EZH2 and promoting differentiation of myogenic precursor cells. The same section describes TNF-induced epigenetic silencing of NOTCH1, but does not establish that p38α mediates that silencing; it also does not specify TNF-receptor binding as the initiating step or directly link this pathway to myotube formation. (LLM, conf=0.85)

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Authors
Tidball, J. G.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Tidball, James G.
ORCID
Tidball, James G.
Venue
Nature Reviews Immunology
Publisher
Springer Science and Business Media LLC
Published
2017-02-06
Volume
17
Issue
3
Pages
165-178
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
DOI
10.1038/nri.2016.150
PMC
PMC5452982
OpenAlex
W2587398364
Cited by
740
References
132
Citations by year
2026: 99 · 2025: 78 · 2024: 97 · 2023: 96 · 2022: 85 · 2021: 89 · 2020: 76 · 2019: 62 · 2018: 44 · 2017: 13
FWCI
4.99
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG041147)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R21AR066817, R01AR066036, R01AR062579)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
muscle regeneration, muscle growth, muscle damage, inflammation, immune system, tissue regeneration, myopathy
MeSH terms
Animals, Humans, Regeneration, Muscle, Skeletal

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