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阻塞性睡眠呼吸暂停低通气综合征与非酒精性脂肪性肝病:新出现的证据和机制。

Obstructive sleep apnea-hypopnea syndrome and nonalcoholic fatty liver disease: emerging evidence and mechanisms.

机构信息

Gradenigo Hospital, Turin, Italy.

出版信息

Semin Liver Dis. 2012 Feb;32(1):49-64. doi: 10.1055/s-0032-1306426. Epub 2012 Mar 13.

Abstract

Obstructive sleep apnea syndrome (OSAS) and nonalcoholic fatty liver disease (NAFLD) are common conditions, frequently encountered in patients with metabolic disorders. OSAS has been associated with an increased risk of cardiovascular and metabolic complications. It has been recently suggested that the chronic intermittent hypoxia of OSAS may also affect the presence and severity of NAFLD. We will critically review experimental and human evidence connecting OSAS to NAFLD pathogenesis, trying to dissect the effect of intermittent hypoxia from that of obesity and associated comorbidities, and examine molecular mechanisms connecting OSAS to liver and metabolic disease in NAFLD, including hypoxia inducible factor (HIF), nuclear factor-kappa B, unfolded protein response, hypoxic adipose tissue inflammation, and their therapeutic potential for NAFLD and its complications, including cirrhosis and hepatocellular carcinoma. Finally, we will provide suggestions for the management of NAFLD patients with suspected OSAS and recommendations for future research.

摘要

阻塞性睡眠呼吸暂停综合征(OSAS)和非酒精性脂肪性肝病(NAFLD)是常见的病症,常发生于代谢紊乱的患者中。OSAS 与心血管和代谢并发症的风险增加有关。最近有人提出,OSAS 的慢性间歇性缺氧也可能影响 NAFLD 的发生和严重程度。我们将批判性地回顾将 OSAS 与 NAFLD 发病机制联系起来的实验和人体证据,试图从肥胖和相关合并症的影响中分离出间歇性缺氧的作用,并研究将 OSAS 与 NAFLD 中的肝脏和代谢疾病联系起来的分子机制,包括缺氧诱导因子(HIF)、核因子-κB、未折叠蛋白反应、缺氧脂肪组织炎症,以及它们在治疗 NAFLD 及其并发症(包括肝硬化和肝细胞癌)方面的潜在应用。最后,我们将为疑似 OSAS 的 NAFLD 患者的管理提供建议,并为未来的研究提出建议。

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