自然杂志 ›› 2026, Vol. 48 ›› Issue (3): 197-204.doi: 10.3969/j.issn.0253-9608.2026.03.004

• 专题综述 • 上一篇    下一篇

阻塞性睡眠呼吸暂停与代谢综合征共病的病理生理机制

赖羽欣①②,黎冰婵①②,刘峰①②   

  1. ①上海交通大学医学院附属第六人民医院 耳鼻咽喉头颈外科,上海 200233;②上海交通大学 耳鼻咽喉科研究所,上海 200233
  • 收稿日期:2026-01-05 出版日期:2026-06-25 发布日期:2026-06-20

Pathological mechanisms in the comorbidity of obstructive sleep apnea and metabolic syndrome

LAI Yuxin①②, LI Bingchan①②, LIU Feng①②   

  1. ① Department of Otolaryngology-Head and Neck Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China; ② Otolaryngology Institute of Shanghai Jiao Tong University, Shanghai 200233, China
  • Received:2026-01-05 Online:2026-06-25 Published:2026-06-20

摘要: 阻塞性睡眠呼吸暂停(obstructive sleep apnea, OSA)与代谢综合征(metabolic syndrome, MetS)高度共病,共同构成代谢以及心血管疾病的重大风险。然而,二者复杂的双向相互作用及临床干预效果的异质性,难以用单一病理生理机制充分阐明。本文围绕OSA与MetS的双向关系,系统综述其关键病理生理环节,包括肥胖作为OSA的始动因素,以及间歇性低氧与睡眠结构异常作为OSA驱动代谢紊乱的核心机制。鉴于OSA与MetS在病理演进中均展现出显著的炎症特征与生物学年龄的老化倾向,本文进一步超越单向作用模型,从衰老与系统性炎症的视角,探讨二者共享的上游驱动机制。本文旨在为深入理解OSA-MetS共病的整合病理生理网络,并为进一步探索针对共同根源的综合管理策略提供新的理论框架。

关键词: 阻塞性睡眠呼吸暂停, 代谢综合征, 睡眠剥夺, 间歇性低氧, 衰老, 系统性低度炎症

Abstract: Obstructive sleep apnea (OSA) and metabolic syndrome (MetS) are highly comorbid conditions, jointly constituting a significant risk factor for metabolic and cardiovascular diseases. However, their complex bidirectional interactions and the heterogeneity of clinical intervention outcomes cannot be fully explained by a single pathological mechanism. Focusing on the bidirectional relationship between OSA and MetS, this article systematically reviews their key pathological links. This includes obesity as an initiating factor for OSA, and intermittent hypoxia along with sleep structure abnormalities as the core mechanisms by which OSA drives metabolic dysregulation. Moving beyond unidirectional models, the article further explores shared upstream driving mechanisms from the perspectives of aging and systemic inflammation. This review aims to provide a deeper understanding of the integrated pathophysiological network underlying OSA-MetS comorbidity and to offer a novel theoretical framework for exploring comprehensive management strategies targeting their common roots.