OSAHS及相关共病中的线粒体功能障碍与氧化应激：机制及潜在靶向治疗策略

文献信息

中文摘要

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）与多系统共病相关，包括心血管疾病、代谢紊乱以及神经、肺和肾脏疾病。目前的研究已揭示，OSAHS及其相关共病的病理生理机制复杂。然而，慢性间歇性缺氧诱导的线粒体功能障碍和氧化应激被认为发挥重要作用。近年来，线粒体功能障碍与氧化应激之间的相互作用机制受到关注，并已成为重要的潜在治疗靶点。未来的递送系统可能改善研究性药物的组织或线粒体靶向性，尽管其在OSAHS中的疗效和安全性仍有待确定。本综述强调线粒体功能障碍与氧化应激之间的相互强化和正反馈环路，并概述了相关治疗药物、其新型递送系统及开发潜力的当前研究。我们的综述旨在为OSAHS相关共病的治疗提供新思路和新方法。

英文摘要

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is associated with multisystem comorbidities, including cardiovascular disease, metabolic disorders, and neurological, pulmonary, and kidney diseases. Current studies have revealed that the pathophysiology of OSAHS and its associated comorbidities is complex. However, chronic intermittent hypoxia-induced mitochondrial dysfunction and oxidative stress are considered to play an important role. In recent years, mechanisms of interaction between mitochondrial dysfunction and oxidative stress have gained attention and have emerged as important potential therapeutic targets. Future delivery systems may improve the tissue or mitochondrial targeting of investigational agents, although their efficacy and safety in OSAHS remain to be established. This review highlights the mutual reinforcement and positive feedback loop between mitochondrial dysfunction and oxidative stress, and provides an overview of the current research on associated therapeutic drugs, their novel delivery systems, and development potential. Our review aims to provide new ideas and methods for the treatment of OSAHS-associated comorbidities.