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Fig. 1 | Stem Cell Research & Therapy

Fig. 1

From: The effect of type 2 diabetes mellitus and obesity on muscle progenitor cell function

Fig. 1

Illustration of the mechanisms for the adipogenic fate determination of FAP in skeletal muscle. Eosinophils infiltrate early during muscle injury, secrete IL-4/IL-13, and subsequently stimulate STAT6 to promote FAP proliferation, while inhibiting its adipogenic differentiation. Activation of Hh signaling also prevents the conversion of FAP to adipocyte. Meanwhile, the direct interaction of FAP with intact myofiber or myo-endothelial cell can prevent its differentiation into adipocyte at resting state. Upon muscle damage, FAPs proliferate dramatically to help debris clearance and induce myogenic cell differentiation. FAP, fibroadipogenic progenitor; STAT6, signal transducer and activator of transcription 6; Hh, hedgehog; TIMP3, tissue inhibitor of metalloproteinases 3; MMP14, matrix metallopeptidase 14

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