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Regulated Necrosis in Pulmonary Disease: A Focus on Necroptosis and Ferroptosis.

To date, increasing evidence suggests the possible involvement of various types of cell death in lung diseases. The recognized regulated cell death (RCD) includes necrotic cell death that is immunogenic, releasing damage-associated molecular patterns (DAMPs) and driving tissue inflammation. Necroptosis is a well-understood form of regulated necrosis that is executed by receptor interacting protein kinase 3 (RIPK3) and the pseudo kinase mixed lineage kinase domain-like protein (MLKL). Ferroptosis is a newly described caspase-independent form of regulated necrosis that is characterized by the increase of detrimental lipid ROS produced via iron-dependent lipid peroxidation. The role of these two cell death pathways differ depending on the disease, cell type, and microenvironment. Moreover, some experimental cell death models have demonstrated shared ferroptotic and necroptotic cell death and the synergistic effect of simultaneous inhibition. This review examines the role of regulated necrotic cell death-particularly necroptosis and ferroptosis-in lung disease pathogenesis, in the context of recent insights into the roles of the key effector molecules of these two cell death pathways.