The First Clinical Medical College of Lanzhou University, Lanzhou, China.
Department of Respiratory and Critical Care Medicine, The First Hospital of Lanzhou University, Lanzhou, China.
Sleep Breath. 2024 Jun;28(3):1051-1065. doi: 10.1007/s11325-024-03001-8. Epub 2024 Feb 3.
Obstructive sleep apnea (OSA) is a common respiratory disorder. Multiple organs, especially the central nervous system (CNS), are damaged, and dysfunctional when intermittent hypoxia (IH) occurs during sleep for a long time. The quality of life of individuals with OSA is significantly impacted by cognitive decline, which also escalates the financial strain on their families. Consequently, the development of novel therapies becomes imperative. IH induces oxidative stress, endoplasmic reticulum stress, iron deposition, and neuroinflammation in neurons. Synaptic dysfunction, reactive gliosis, apoptosis, neuroinflammation, and inhibition of neurogenesis can lead to learning and long-term memory impairment. In addition to nerve injury, the role of IH in neuroprotection was also explored. While causing neuron damage, IH activates the neuronal self-repairing mechanism by regulating antioxidant capacity and preventing toxic protein deposition. By stimulating the proliferation and differentiation of neural stem cells (NSCs), IH has the potential to enhance the ratio of neonatal neurons and counteract the decline in neuron numbers. This review emphasizes the perspectives and opportunities for the neuroprotective effects of IH and informs novel insights and therapeutic strategies in OSA.
阻塞性睡眠呼吸暂停（OSA）是一种常见的呼吸系统疾病。当睡眠中长时间出现间歇性低氧（IH）时，多个器官，尤其是中枢神经系统（CNS），会受到损伤和功能障碍。OSA 患者的认知能力下降会显著影响其生活质量，同时也会给家庭带来经济负担。因此，开发新的治疗方法迫在眉睫。IH 会导致神经元中氧化应激、内质网应激、铁沉积和神经炎症。突触功能障碍、反应性神经胶质增生、细胞凋亡、神经炎症和神经发生抑制可导致学习和长期记忆障碍。除了神经损伤，IH 在神经保护中的作用也得到了探索。虽然 IH 会导致神经元损伤，但它可以通过调节抗氧化能力和防止有毒蛋白沉积来激活神经元的自我修复机制。IH 通过刺激神经干细胞（NSCs）的增殖和分化，有可能增加新生神经元的比例，抵消神经元数量的下降。本综述强调了 IH 的神经保护作用的观点和机会，并为 OSA 提供了新的见解和治疗策略。
