肥胖、睡眠呼吸暂停与癌症再探讨

文献信息

中文摘要

背景： 阻塞性睡眠呼吸暂停（OSA）、肥胖与癌症构成一个相互关联的病理生理三联征，对发病率和死亡率具有重要影响。肥胖是OSA和肿瘤发生的共同上游驱动因素，而OSA通过间歇性缺氧、睡眠碎片化、全身性炎症、氧化应激、免疫失调和交感神经激活独立发挥作用。新出现的证据将OSA相关低氧血症与癌症发生、进展和治疗反应联系起来，其中低氧负荷和夜间血氧饱和度下降指标在预测癌症相关结局方面优于呼吸暂停低通气指数。机制研究进展表明，免疫检查点信号、细胞外基质重塑和代谢-肝脏通路是OSA相关肿瘤发生的关键介质。流行病学研究支持OSA与多种恶性肿瘤之间的关联独立于肥胖，尽管残余混杂仍然是一个挑战。在治疗方面，持续气道正压通气可能减轻低氧血症相关通路，而减重手术和GLP-1/GIP受体激动剂具有同时降低肥胖、OSA严重程度和癌症风险的潜力。需要整合低氧血症表型分析、免疫谱分析和靶向干预的精准医学方法来优化预防和治疗策略。

英文摘要

Obstructive sleep apnea (OSA), obesity, and cancer constitute an interconnected pathophysiological triad withi mportant implications for morbidity and mortality. Obesity is a major upstream driver of both OSA and tumorigenesis, while OSA contributes independently through intermittent hypoxia, sleep fragmentation, systemici nflammation, oxidative stress, immune dysregulation, and sympathetic activation. Emerging evidence links OSA-associated hypoxemia to cancer initiation, progression, and treatment response, with hypoxic burden and nocturnal oxygen desaturation metrics outperforming the apnea-hypopnea index in predicting cancer-related outcomes. Mechanistic advances implicate immune checkpoint signaling, extracellular matrix remodeling, and metabolic-hepatic pathways as key mediators of OSA-related oncogenesis. Epidemiological studies support associations between OSA and several malignancies independent of obesity, although residual confounding remains a challenge. Therapeutically, continuous positive airway pressure may mitigate hypoxemia-related pathways, whereas bariatric surgery and GLP-1/GIP receptor agonists off er the potential to simultaneously reduce obesity, OSA severity, and cancer risk. Precision medicine approaches integrating hypoxemia phenotyping, immune profi ling, and targeted interventions are needed to optimize prevention and treatment strategies.