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
. 2025:1478:185-212.
doi: 10.1007/978-3-031-88361-3_9.

Skeletal Muscle Damage and Inflammation

Tyrone A Washington  1 , Eleanor R Schrems  2
Affiliations
Review

Skeletal Muscle Damage and Inflammation

Tyrone A Washington et al. Adv Exp Med Biol. 2025.

Abstract

Skeletal muscle is an extremely plastic tissue that can respond to a variety of insults. If the insult is sufficient, it may reduce damage to the skeletal muscle. Damage to skeletal muscle is associated with an inflammatory response. This inflammatory response is required for optimal regeneration. There are several models used to induce damage to skeletal muscle from eccentric muscle actions to myotoxin injections. While the method of inducing damage may vary the inflammatory response is similar. Upon damage, circulating immune cells are activated and infiltrate the tissue. The first to arrive is the neutrophil followed by the macrophage. The neutrophil clears debris and releases pro-inflammatory signals which facilitate the recruitment of macrophages. Macrophages are recruited and begin as pro-inflammatory macrophages (M1) continuing to facilitate the clearance of debris before macrophage polarization occurs in which they become anti-inflammatory macrophage (M2). The anti-inflammatory macrophages facilitate the myogenic response critical for optimal regeneration. Disruptions to the inflammatory response will directly affect the ability of the skeletal muscle to recover from injury.

Keywords: Injury; Macrophage; Natural killer cells; Neutrophils.

PubMed Disclaimer

References

    1. Allen DG, Lamb GD, Westerblad H (2008) Skeletal muscle fatigue: cellular mechanisms. Physiol Rev 88(1):287–332. https://doi.org/10.1152/physrev.00015.2007 - DOI - PubMed
    1. Amulic B, Cazalet C, Hayes GL, Metzler KD, Zychlinsky A (2012) Neutrophil function: from mechanisms to disease. Annu Rev Immunol 30:459–489. https://doi.org/10.1146/annurev-immunol-020711-074942 - DOI - PubMed
    1. Ancuta P, Weiss L, Haeffner-Cavaillon N (2000) CD14+CD16++ cells derived in vitro from peripheral blood monocytes exhibit phenotypic and functional dendritic cell-like characteristics. Eur J Immunol 30(7):1872–1883 - PubMed
    1. Anders HJ, Schaefer L (2014) Beyond tissue injury-damage-associated molecular patterns, toll-like receptors, and inflammasomes also drive regeneration and fibrosis. J Am Soc Nephrol 25(7):1387–1400. https://doi.org/10.1681/ASN.2014010117 - DOI - PubMed - PMC
    1. Armstrong RB, Ogilvie RW, Schwane JA (1983) Eccentric exercise-induced injury to rat skeletal muscle. J Appl Physiol Respir Environ Exerc Physiol 54(1):80–93. https://doi.org/10.1152/jappl.1983.54.1.80 - DOI - PubMed

LinkOut - more resources