Ferroptosis is a non-apoptotic mode of cell death characterized by iron-dependent lipid peroxides accumulation-induced membrane lipid peroxidation and mitochondrial atrophy, and differed from other programmed cell deaths in morphological and biochemical properties. Ferroptosis is regulated by a variety of metabolic pathways, involved in acute lung injury induced by hemorrhagic shock, ischemia-reperfusion, sepsis, and radiation. This article reviews the main regulatory mechanisms of ferroptosis and its role in the pathogenesis of acute lung injury in various animal models, with the aim of providing new strategies for the prevention and treatment of acute lung injury.