阻塞性睡眠呼吸暂停对皮肤伤口愈合的影响——从临床前视角到临床证据：一篇叙述性综述
The impact of obstructive sleep apnea on skin wound healing - from preclinical perspective to clinical evidence: A narrative review.
文献信息
| PMID | 42773334 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Łukasz Mazurek |
| 作者单位 | Department of Otorhinolaryngology, Faculty of Medicine and Dentistry, Medical University of Warsaw, Warsaw, 02-091, Poland. |
| 期刊 | Sleep & breathing = Schlaf & Atmung |
| SCI 分区 | Q3 |
| IF | 2.8 |
| 研究类型 | 综述 Meta · 临床 |
| 所属专科 | 鼻科 |
中文摘要
目的： 充足的组织氧合对于有效的皮肤伤口愈合至关重要。缺氧会导致愈合受损和慢性伤口形成。阻塞性睡眠呼吸暂停（OSA）影响全球近十亿成年人，且高达80%的病例未被诊断。OSA引起间歇性缺氧（IH），在睡眠期间反复出现氧饱和度下降和再氧合的循环。IH激活的分子通路与急性和慢性缺氧所诱导的不同。我们提出OSA可能通过两种方式导致伤口愈合受损。间接地，通过促进糖尿病、高血压和肥胖等合并症。直接地，通过IH及其在细胞和组织水平的影响。
方法： 检索了PubMed/MEDLINE、Scopus和Web of Science截至2026年8月关于OSA、IH和伤口愈合的临床前和临床研究。
结果： 据我们所知，这是第一篇整合该主题的细胞机制、临床前证据和临床数据的综述。我们描述了可能促进伤口愈合受损的IH驱动机制，包括抗氧化能力降低、持续性炎症、交感神经激活和内皮功能障碍。临床前证据有限，主要来自体外划痕实验。它显示IH延迟伤口闭合，下调HIF-2α和VEGF，并使巨噬细胞向促炎表型转变。临床数据也有限且异质性大。在糖尿病足溃疡中，高OSA风险使愈合不良的风险加倍。CPAP后溃疡愈合改善仅在小病例系列中有描述。
结论： 鉴于其高患病率和诊断不足，OSA可能是伤口愈合受损的一个被忽视且潜在可修改的因素。
英文摘要
PURPOSE: Adequate tissue oxygenation is essential for effective skin wound healing. Hypoxia contributes to impaired healing and chronic wound formation. Obstructive sleep apnea (OSA) affects nearly one billion adults worldwide, and up to 80% of cases remain undiagnosed. OSA causes intermittent hypoxia (IH), with repetitive cycles of oxygen desaturation and reoxygenation during sleep. The molecular pathways activated by IH differ from those induced by acute and chronic hypoxia. We propose that OSA may contribute to impaired wound healing in two ways. Indirectly, by promoting comorbidities such as diabetes, hypertension, and obesity. Directly, through IH and its effects at the cellular and tissue level.
METHODS: PubMed/MEDLINE, Scopus, and Web of Science were searched through August 2026 for preclinical and clinical studies on OSA, IH, and wound healing.
RESULTS: To our knowledge, this is the first review to integrate cellular mechanisms, preclinical evidence, and clinical data on this topic. We describe the IH-driven mechanisms that may contribute to impaired wound healing, including reduced antioxidant capacity, sustained inflammation, sympathetic activation, and endothelial dysfunction. Preclinical evidence is limited and mostly derives from in vitro scratch assays. It shows that IH delays wound closure, downregulates HIF-2α and VEGF, and shifts macrophages toward a pro-inflammatory phenotype. Clinical data are also limited and heterogeneous. In diabetic foot ulcers, high OSA risk doubled the risk of poor healing. Improved ulcer healing after CPAP has been described only in a small case series.
CONCLUSION: Given its high prevalence and underdiagnosis, OSA may be an overlooked and potentially modifiable factor in impaired wound healing.