Reverse of liver fibrosis by inducing ferroptosis by bioactivated compounds in HSCs. Chrysophanol, liraglutide, wogonoside, danshensu relieve liver fibrosis by inhibiting SLC7A11 to induce ferroptosis. Artemether, wogonoside, erastin, or sorafenib relieve liver fibrosis by acting on p53 to induce ferroptosis, which is involved in regulating ferroptosis via systemic XC. Dihydroartemisinin and curcumol targeting acts on NCOA4, induces ferroptosis, and alleviates liver fibrosis. ATG5 plasmid and NCOA4 plasmid are able to promote the induction of iron death by dihydroartemisinin. Solafennib induced ferroptosis in HIF-1α through the HIF-1α/SLC7A11 pathway. GSK2656157 can promote solafennib to induce ferroptosis in HSCs. Acrylamide, danshensu, isoliquiritigenin, decursin, and celastrol inhibit GPX 4, thereby inducing ferroptosis in HSCs to alleviate liver fibrosis. Sorafenib, erastin, and RSL3 ZFP36 siRNA relieve liver fibrosis by acting on ZFP36 to induce ferroptosis. ATG16L1 mRNA can activate the autophagic ferritin, leading to the ferroptosis of HSCs. Artemether induced ferroptosis in HSCs to relieve liver fibrosis by upregulating IRTF2. Isoliquiritigenin induced ferroptosis in HSCs to relieve liver fibrosis by inhibiting TFR. Ellagic acid downregulates FPN 1 to induce ferroptosis and relieve liver fibrosis. BECN1 mRNA promotes the activation of autophagy to induce ferroptosis in HSCs. m6A induces ferroptosis in HSCs by stabilizing BECN1 mRNA to trigger autophagy activation. NaAsO2 can increase the level of iron ions to induce the iron death of HSCs.
