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) as a regulator of adipogenic and fibrogenic FAP differentiation. In the context of fibrogenic FAP differentiation, ADAMTSL2 inhibited the differentiation of primary mouse and human FAPs into fibroblasts in a transforming growth factor β (TGF-β)-dependent manner. Together with our previous data, a model emerges where ADAMTSL2 has a dual role in skeletal muscle biology, a pro-myogenic role, where ADAMTSL2 promotes myogenic muscle stem cell differentiation, and a TGF-β-dependent anti-fibrotic role where ADAMTSL2 attenuates FAP-to-fibroblast differentiation.
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Redhead et al. (2025) studied this question.
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