Skeletal muscle atrophy has been characterizedas a state of uncontrolled inflammation and oxidative stress that escalates the protein catabolism. Recent advancement supportsthat impinging signaling molecules in the muscle fibers controlled throughtoll-like receptors (TLR). Activated TLR signalingpathways have been identified as inhibitors of muscle mass and provoke the settings for muscle atrophy. Among them, mainly TLR2 and TLR4 manifest their presence to exacerbate the release of the pro-inflammatory cytokine to deform the synchronized muscle programming. The present review enlightens the TLR signaling mediated muscle loss and their interplay betweeninflammationand skeletal muscle growth.
Keywords: Toll-like receptors, skeletal muscle atrophy, inflammation, oxidative stress, pro-inflammatory cytokines
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