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已发表论文
铁死亡在阻塞性睡眠呼吸暂停综合征病理生理学中的潜在机制
Received 30 June 2025
Accepted for publication 18 October 2025
Published 22 November 2025 Volume 2025:17 Pages 3033—3051
DOI https://doi.org/10.2147/NSS.S549883
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Prof. Dr. Ahmed BaHammam
Xiangxia Zeng,1 Nuofu Zhang2
1Department of Nutrition, School of Public Health, Guangzhou Medical University, Guangzhou, 511436, People’s Republic of China; 2Sleep Medicine Center, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, National Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 511436, People’s Republic of China
Correspondence: Nuofu Zhang, Sleep Medicine Center, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, National Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 511436, People’s Republic of China, Tel +86-20-83062850, Email nfzhanggird@163.com
Abstract: 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.
Keywords: obstructive sleep apnea syndrome, ferroptosis, oxidative stress, iron metabolism, inflammation, cardiovascular disease, neurodegeneration
1Department of Nutrition, School of Public Health, Guangzhou Medical University, Guangzhou, 511436, People’s Republic of China; 2Sleep Medicine Center, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, National Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 511436, People’s Republic of China
Correspondence: Nuofu Zhang, Sleep Medicine Center, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, National Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 511436, People’s Republic of China, Tel +86-20-83062850, Email nfzhanggird@163.com
Abstract: 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.
Keywords: obstructive sleep apnea syndrome, ferroptosis, oxidative stress, iron metabolism, inflammation, cardiovascular disease, neurodegeneration