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The muscle–immune relationship is not unidirectional but represents a dynamic, bidirectional crosstalk: while exercise-induced myokines (including heat shock proteins, interleukins, and metabolic regulators) reprogram immune cell phenotypes and suppress inflammaging, immune-derived inflammatory cytokines (TNF-α, IL-6, IL-1β) conversely drive muscle wasting in aging, creating a vicious cycle that accelerates sarcopenia and immunosenescence [17,121]
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