Ferroptosis is a non-apoptotic mode of cell death characterized by iron-dependent lipid-peroxideaccumulation-induced membrane lipid peroxidation and mitochondrial atrophy. It differs from other programmed cell deaths in its morphological and biochemical properties. Ferroptosis is regulated by a variety of metabolic pathways that are involved in the 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.