In the present study, a dramatic increase in levels of intracellular iron accumulation and 4-HNE (an activator of ferroptosis) but decreased levels of GPX4 (an inhibitor of ferroptosis) were observed in lung tissue of experimental MA-ALI mice compared to naive mice, which were rescued by administration of the Piezo1 inhibitor GsMTx4, indicating that ferroptosis could be involved in mediating the severity of MA-ALI. This evidence concerns the gene PIEZO1 and acute respiratory distress syndrome.