Ferroptosis is a unique way of regulated cell death characterized by iron-dependent and excessive accumulation of lipid peroxides. It is greatly different from apoptosis, necrosis, autophagy, and other forms of cell death in morphology, biology, and genetics. The metabolism of iron, lipid and amino acid and other signaling pathways are closely related to ferroptosis. It is closely associated with the pathological processes of diseases such as cancer, inflammation, neurodegeneration, liver and kidney injury, and ischemia/reperfusion injury. Acute respiratory distress syndrome (ARDS) is an inflammatory disease of the lung that seriously threatens human life and health with high incidence and mortality. The pathways involved in lung injury pathogenesis and repair have been broadened in recent years. Therapies targeting ventilation-induced lung injury have consistently proven beneficial for ARDS patients, but there is still a lack of effective drug treatment. The global pandemic of the coronavirus disease 2019 has made ARDS even more severe. It is urgent to further explore its mechanism at cellular and molecular levels and develop new therapies. This article reviews the definition and mechanism of ferroptosis and its role in ARDS from basic to clinics.