ArticleFrontiers in immunology2026
Regenerating myofiber with activating of TGF-β signaling contributes to macrophage efferocytosis through enhancing Tregs response in inflamed muscle.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: This study aimed to investigate the role of myofiber-specific TGF-β signaling in the development of muscle inflammation by modulating Treg-cell-mediated macrophage efferocytosis. Methods: CTX-induced muscle injury was performed in the tibialis anterior (TA) of control (TGF-βr2 Results: Deficiency in muscle TGF-β signaling resulted in more severe muscle inflammation, characterized by an increased number of M1 macrophages and a decreased number of M2 macrophages. Notably, the absence of muscle TGF-β signaling impaired the efferocytic capacity of macrophages and reduced the proportion of Tregs in inflamed muscle. Further, we monitored that activation of intrinsic TGF-β signaling suppresses myofiber IL-6 production, which in turn impacted on IL-13 production from Tregs accumulated in damaged muscle. This ultimately facilitates IL-10-STAT3-Vav1-mediated macrophage efferocytosis in inflamed muscle. Conclusions: Our findings establish a link between muscle-specific TGF-β signaling, myokine IL-6, Tregs derived IL-13 and macrophage efferocytosis in inflamed muscle. These results suggest that therapeutic targeting of this axis may hold promise for promoting muscle regeneration.
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