Ou Yanru, Wang Xiufang, Zong Dandan, Ouyang Ruoyun
Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China.
Cell Biosci. 2025 Jun 20;15(1):85. doi: 10.1186/s13578-025-01418-6.
Cognitive impairment (CI) is a significant and extraordinary complication of obstructive sleep apnea (OSA) patients. Programmed cell death (PCD) is an active and ordered process regulated by genes. A growing number of studies find that PCD is responsible for cognitive dysfunction and plays an important role in various neurological diseases, which involve apoptosis, necroptosis, pyroptosis, ferroptosis, and cell death associated with autophagy. However, the influence of PCD on OSA-CI remains unclear. We summarized the relevant studies that discussed the involvement of PCD in the CI of OSA and aimed to clarify the underlying mechanisms. Intermittent hypoxia (IH)-induced PCD had a critical effect on the mechanisms that produced the ultimate neurological deficit in OSA, and the PCD involved mainly included apoptosis, autophagy, ferroptosis, and pyroptosis. IH regulates PCD directly or through specific pathways, and drugs targeting related molecules have the potential to improve cognitive function. These findings enrich the pathogenesis of OSA-CI and provide new therapeutic insights.
认知障碍（CI）是阻塞性睡眠呼吸暂停（OSA）患者一种严重且特殊的并发症。程序性细胞死亡（PCD）是一个由基因调控的主动且有序的过程。越来越多的研究发现，PCD导致认知功能障碍，并在各种神经疾病中起重要作用，这些疾病包括细胞凋亡、坏死性凋亡、细胞焦亡、铁死亡以及与自噬相关的细胞死亡。然而，PCD对OSA-CI的影响仍不清楚。我们总结了讨论PCD参与OSA患者CI的相关研究，旨在阐明其潜在机制。间歇性缺氧（IH）诱导的PCD对OSA患者产生最终神经功能缺损的机制具有关键作用，且涉及的PCD主要包括细胞凋亡、自噬、铁死亡和细胞焦亡。IH直接或通过特定途径调节PCD，靶向相关分子的药物具有改善认知功能的潜力。这些发现丰富了OSA-CI的发病机制，并提供了新的治疗思路。
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