Ferroptosis: molecular mechanisms, pathophysiology, and role in pediatric pulmonary diseases.
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Ferroptosis is a distinct form of programmed cell death characterized by iron-dependent oxidative stress and the accumulation of intracellular reactive oxygen species. This process involves multiple structural alterations, such as rupture of the outer mitochondrial membrane, reduced mitochondrial volume, and the decrease or disappearance of cristae. Additionally, ferroptosis is accompanied by iron overload and heightened lipid peroxidation (LPO). Although ferroptosis has been extensively investigated in various adult diseases, including infectious diseases, neurodegenerative disorders, cancers, and cardiovascular conditions, its role in pediatric respiratory diseases remains unclear. The molecular mechanisms of ferroptosis, particularly iron overload and LPO, are closely linked to the oxidative stress and inflammatory responses commonly observed in respiratory diseases. This review aims to summarize the fundamental processes and regulatory mechanisms of ferroptosis and to explore its potential relevance in pediatric respiratory diseases. By analyzing these mechanisms in depth, we can not only contribute to elucidating the pathophysiological features of pediatric respiratory illnesses but also provide novel insights and therapeutic targets for treatment strategies focusing on ferroptosis, offering new directions for clinical prevention and therapy in respiratory diseases.