Toll-like receptor signalling in regenerative myogenesis: Friend and foe

Abstract

Skeletal muscle regeneration in normal and diseased muscle is regulated by multiple factors and cells present in the injured muscle microenvironment. In addition to muscle progenitor cells, several immunocytes participate in the regenerative response. Among them, macrophages are one of the most important components of the immune response which govern step-wise progression of muscle regeneration. The initial role of macrophages is to phagocytize muscle cell debris and later through their transition to an anti-inflammatory phenotype, they promote regeneration. However, in several genetic muscle disorders, continuous muscle injury disrupts the balance between proinflammatory and anti-inflammatory macrophages leading to overall inflammatory milieu and inhibition of muscle regeneration. Accumulating evidence suggests that toll-like receptor (TLR)-mediated signalling plays an important role in the regulation of macrophage phenotypes during regenerative myogenesis in response to both acute and chronic muscle injury. Here, we discuss the role of TLR signalling in regulating macrophage phenotypes and skeletal muscle regeneration in healthy and diseased muscle.

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