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Extracellular vesicles (EVs) serve as key facilitators mediating intercellular communication in skeletal muscle, but the upstream mechanisms regulating their secretion remain incompletely understood. Using proteomic screening, we identified CXCL12 as a candidate HSF1-associated downstream factor. Functional assays showed that CXCL12 promoted C2C12 myoblast proliferation, restrained myogenic differentiation in a stage-dependent manner, and enhanced sEV secretion, accompanied by altered expression of early endosome- and MVB-associated markers. Functionally, CXCL12 knockdown attenuated the HSF1-induced increase in sEV secretion and the upregulation of EEA1 and CD63 protein levels, whereas exogenous recombinant CXCL12 partially restored EEA1 and CD63 expression in the skeletal muscle of muscle-specific HSF1 knockout mice. Collectively, these results are consistent with a model in which CXCL12 is associated with sEV secretion in coordination with changes in early endosome- and MVB-associated protein abundance, suggesting a previously underappreciated role for CXCL12 in vesicle trafficking in the skeletal muscle microenvironment.
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Dong et al. (2026) studied this question.
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