Ferroptosis as a Potential Mechanism in the Pathophysiology of Obstructive Sleep Apnea Syndrome

Obstructive Sleep Apnea Syndrome (OSAS) is a prevalent sleep disorder characterized by recurrent upper airway obstruction, resulting in intermittent hypoxia, oxidative stress, and systemic inflammation. Ferroptosis, an iron-dependent form of regulated cell death triggered by lipid peroxidation, has recently been proposed as a potential contributor to the tissue injury observed in OSAS. OSAS appears to aggravate disturbances in iron homeostasis and oxidative imbalance, both of which may converge to exacerbate disease pathophysiology. However, the precise mechanisms linking ferroptosis to OSAS remain largely speculative. Emerging evidence from experimental studies indicates that ferroptosis-related genes and pathways might be involved in the cardiovascular, neurological, and renal complications associated with OSAS. This review summarizes current knowledge regarding oxidative stress and iron metabolism under intermittent hypoxia, explores the potential regulatory mechanisms of ferroptosis, and discusses its hypothesized contribution to OSAS-related organ injury. While targeting ferroptosis may represent a promising research direction, the current evidence remains preliminary and predominantly experimental. Further mechanistic and clinical investigations are essential to clarify whether ferroptosis plays a causal role in OSAS pathogenesis and to evaluate its translational relevance.