Salvianolic acid B (Sal B) alleviates liver fibrosis by targeting extracellular matrix protein 1 (Ecm1) and inhibiting hepatocyte ferroptosis. In this study, liver fibrosis was induced in mice using carbon tetrachloride (CCl4), and Sal B treatment significantly reduced fibrosis. Ecm1 deletion in hepatocytes abolished the antifibrotic effect of Sal B, indicating that Ecm1 is a key target. Mechanistically, Sal B upregulates Ecm1, which protects against hepatocyte ferroptosis by interacting with xCT. Sal B treatment reduced ferroptosis markers and improved liver fibrosis in mice. In vitro experiments confirmed that Sal B binds to Ecm1 and inhibits ferroptosis. The interaction between Ecm1 and xCT regulates hepatocyte ferroptosis, and Sal B inhibits this process by upregulating Ecm1. These findings suggest that Sal B alleviates liver fibrosis by targeting Ecm1 and inhibiting hepatocyte ferroptosis. The study highlights a novel mechanism by which Sal B exerts its antifibrotic effects.Salvianolic acid B (Sal B) alleviates liver fibrosis by targeting extracellular matrix protein 1 (Ecm1) and inhibiting hepatocyte ferroptosis. In this study, liver fibrosis was induced in mice using carbon tetrachloride (CCl4), and Sal B treatment significantly reduced fibrosis. Ecm1 deletion in hepatocytes abolished the antifibrotic effect of Sal B, indicating that Ecm1 is a key target. Mechanistically, Sal B upregulates Ecm1, which protects against hepatocyte ferroptosis by interacting with xCT. Sal B treatment reduced ferroptosis markers and improved liver fibrosis in mice. In vitro experiments confirmed that Sal B binds to Ecm1 and inhibits ferroptosis. The interaction between Ecm1 and xCT regulates hepatocyte ferroptosis, and Sal B inhibits this process by upregulating Ecm1. These findings suggest that Sal B alleviates liver fibrosis by targeting Ecm1 and inhibiting hepatocyte ferroptosis. The study highlights a novel mechanism by which Sal B exerts its antifibrotic effects.