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慢性间歇性缺氧诱导的神经损伤:病理生理学、神经退行性变影响及治疗见解

Chronic Intermittent Hypoxia-Induced Neural Injury: Pathophysiology, Neurodegenerative Implications, and Therapeutic Insights.

作者信息

Jia Nan-Nan, Yao Meng-Fan, Zhu Chun-Xue, He Mei-Juan, Zhu Hai-Feng, Chen Zun-Yu, Huang Han-Peng, Qiao Chen

机构信息

The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, Jiangsu, China.

Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.

出版信息

CNS Neurosci Ther. 2025 Apr;31(4):e70384. doi: 10.1111/cns.70384.

Abstract

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a sleep-related respiratory disorder that poses a global threat to human health. Chronic intermittent hypoxia (CIH) is its main pathological feature. With the advancements in medical research, the study of CIH-induced neural injury has gained increasing attention. Studies have shown that CIH can lead to or aggravate neuroinflammation and apoptosis by increasing blood-brain barrier (BBB) permeability, promoting oxidative stress, activating glial cells, and triggering multiple signaling pathways, ultimately resulting in neural injury. These processes contribute to the development of Alzheimer's disease, Parkinson's disease, and stroke. This review aims to summarize the progress in CIH-induced neural injury and explore various underlying mechanisms, with the goal of providing new insights for the development of therapeutic interventions targeting CIH-related neural damage.

摘要

阻塞性睡眠呼吸暂停低通气综合征(OSAHS)是一种与睡眠相关的呼吸系统疾病,对人类健康构成全球威胁。慢性间歇性缺氧(CIH)是其主要病理特征。随着医学研究的进展,CIH诱导的神经损伤研究越来越受到关注。研究表明,CIH可通过增加血脑屏障(BBB)通透性、促进氧化应激、激活胶质细胞和触发多种信号通路,导致或加重神经炎症和细胞凋亡,最终导致神经损伤。这些过程促进了阿尔茨海默病、帕金森病和中风的发展。本综述旨在总结CIH诱导神经损伤的研究进展,并探讨各种潜在机制,以期为针对CIH相关神经损伤的治疗干预措施的开发提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0147/12012570/648056741d27/CNS-31-e70384-g002.jpg

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