〔Abstract〕 Objective To investigate the mechanism by which Erastin affects ferroptosis in lung fibroblasts. Methods Mouse lung fibroblasts(C57/B6-L) were treated with varying concentrations of the iron death inducer Erastin. Cell viability was assessed using the cell counting Kit-8(CCK-8) assay. Oxidative stress levels were visualized using a fluorescence microscope, and the expression of proteins related to the mitogen-activated protein kinase(MAPK) signaling pathway was analyzed using Western blot. Additionally, the p38 and extracellular regulated protein kinase(ERK) inhibitors SB203580 and U0126 were employed to further elucidate the mechanism by which Erastin induces iron death in lung fibroblasts. Results At a concentration of 100 μmol/L, Erastin effectively induced ferroptosis in lung fibroblasts, leading to an upregulation of oxidative stress. Furthermore, the phosphorylation levels of p38 and ERK proteins in the MAPK pathway were elevated(P<0.05). The addition of SB203580 and U0126 inhibitors resulted in a significant reduction in oxidative stress levels and a notable increased in cell activity in lung fibroblasts(P<0.05). Conclusion It can be concluded that Erastin induces ferroptosis in lung fibroblasts, potentially through the mediation of oxidative stressviathe MAPK signaling pathway.