
The study demonstrated that succinate and its receptor, SUCNR1, promote fibrosis in IPF by increasing fibrotic markers and exacerbating fibroblast-myofibroblast transition. In vitro, succinate treatment elevated collagen and α-SMA expression in IPF fibroblasts. In vivo, succinate worsened lung fibrosis and weight loss in bleomycin-treated mice. Targeting SUCNR1 could offer a new therapeutic approach for managing IPF.
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