Nonmuscle cells play central roles in muscle repair and regeneration during the inflammation that follows muscle injury, although many aspects of the mechanisms by which inflammatory cells are attracted to injury sites and activated are unknown. Current evidence indicates that substances released from injured muscle can act as "wound hormones" that initiate inflammation. Most evidence supports the view that mononucleated cells that normally reside in muscle are activated by the injury, and then provide the chemotactic signal to circulating inflammatory cells. Three subsequent stages of inflammation can be identified, according to differences in the populations of inflammatory cells. First, neutrophils rapidly invade the injury site and promote inflammation by releasing cytokines that can attract and activate additional inflammatory cells. In at least some muscle injuries, neutrophils may further damage the injured muscle by releasing oxygen-free radicals that can damage cell membranes. Next, there is an increase in macrophages that invade damaged muscle fibers and phagocytose debris. Finally, there is an increase in a second subpopulation of macrophages that are associated with muscle regeneration. Although many of the potential mediators that underlie the proliferation, invasion, and activation of these inflammatory cell populations are known, few have been demonstrated conclusively to function in injured muscle in vivo.
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Nonmuscle cells play central roles in muscle repair and regeneration during the inflammation that follows muscle injury, although many aspects of the mechanisms by which inflammatory cells are attracted to injury sites and activated are unknown. Current evidence indicates that substances released from injured muscle can act as "wound hormones" that initiate inflammation. Most evidence supports the view that mononucleated cells that normally reside in muscle are activated by the injury, and then provide the chemotactic signal to circulating inflammatory cells. Three subsequent stages of inflammation can be identified, according to differences in the populations of inflammatory cells. First, neutrophils rapidly invade the injury site and promote inflammation by releasing cytokines that can attract and activate additional inflammatory cells. In at least some muscle injuries, neutrophils may further damage the injured muscle by releasing oxygen-free radicals that can damage cell membranes. Next, there is an increase in macrophages that invade damaged muscle fibers and phagocytose debris. Finally, there is an increase in a second subpopulation of macrophages that are associated with muscle regeneration. Although many of the potential mediators that underlie the proliferation, invasion, and activation of these inflammatory cell populations are known, few have been demonstrated conclusively to function in injured muscle in vivo.
Copyright remains with the authors and publisher.