Abstract
Acute respiratory distress syndrome (ARDS) is an acute and uncontrolled pulmonary inflammation caused by various insults. Cell death is a critical mechanism in the pathogenesis of ARDS. Ferroptosis, a novel form of cell death defined as iron-mediated lipid peroxidation, has been shown to play a role in the pathogenesis of ARDS. Additionally, pyroptosis and necroptosis are also involved in the pathophysiological process of ARDS. The crosstalk among ferroptosis, pyroptosis, and necroptosis is getting increasing attention. Therefore, this review will mainly summarize the molecular mechanisms and central pathophysiological role of ferroptosis in ARDS. We will also discuss our understanding of pyroptosis and necroptosis as they pertain to the pathogenesis of ARDS. Furthermore, we also describe the pathological processes that engage crosstalk among ferroptosis, pyroptosis, and necroptosis. We consider that individual pathways of ferroptosis, pyroptosis, and necroptosis are highly interconnected and can compensate for one another to promote cell death.