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缺氧与非酒精性脂肪性肝病。

Hypoxia and non-alcoholic fatty liver disease.

机构信息

Department of Endocrinology and Metabolism, The Institute of Developmental Sciences, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, U.K.

出版信息

Clin Sci (Lond). 2009 Dec 14;118(6):397-400. doi: 10.1042/CS20090565.

Abstract

NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation.

摘要

非酒精性脂肪性肝病(NAFLD)代表了与 2 型糖尿病和心血管疾病风险增加相关的一系列脂肪性肝病。脂肪性肝病谱包括单纯性脂肪变性、伴有炎症的脂肪变性[即非酒精性脂肪性肝炎(NASH)]、伴有炎症和纤维化的脂肪性肝病(严重 NASH)和肝硬化。导致 NASH 的分子机制是相当多的研究主题,因为更好地了解 NASH 的发病机制将为一种迄今难以治疗的疾病带来新的治疗方法。在本期《临床科学》中,Piguet 及其同事研究了缺氧对 PTEN(第 10 号染色体缺失的磷酸酶和张力蛋白同源物)缺陷小鼠的影响,该小鼠模型会发展为非酒精性脂肪性肝病。作者表明,短时间(7 天)暴露于缺氧会加重非酒精性脂肪性肝病表型,导致肝脏发生变化,符合伴有脂肪生成增加和炎症的 NASH。

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