Taken together, the experimental findings suggest that SDH suppression, extracellular succinate accumulation, and SUCNR-1 upregulation form a vicious cycle to enhance HSC activation and myofibroblast transdifferentiation and perpetuate myofibroblast-mediated liver fibrosis following hepatic damage by viral infection, toxin exposure, and/or a high-fat diet (Figure 4). The gene discussed is SUCNR1; the disease is Hepatic fibrosis.