内质网应激与非酒精性脂肪性肝病中的未折叠蛋白反应。
Endoplasmic reticulum stress and the unfolded protein response in nonalcoholic fatty liver disease.
机构信息
Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado 80523-1571, USA.
出版信息
Antioxid Redox Signal. 2011 Jul 15;15(2):505-21. doi: 10.1089/ars.2010.3790. Epub 2011 Apr 26.
Abstract
The underlying causes of nonalcoholic fatty liver disease (NAFLD) are unclear, although recent evidence has implicated the endoplasmic reticulum (ER) in both the development of steatosis and progression to nonalcoholic steatohepatitis. Disruption of ER homeostasis, often termed "ER stress," has been observed in liver and adipose tissue of humans with NAFLD and/or obesity. Importantly, the signaling pathway activated by disruption of ER homeostasis, the unfolded protein response, has been linked to lipid biosynthesis, insulin action, inflammation, and apoptosis. Therefore, understanding the mechanisms that disrupt ER homeostasis in NAFLD and the role of ER-mediated signaling have become topics of intense investigation. The present review will examine the ER and the unfolded protein response in the context of NAFLD.
摘要
非酒精性脂肪性肝病 (NAFLD) 的根本原因尚不清楚，尽管最近的证据表明内质网 (ER) 既参与了脂肪变性的发展，也参与了向非酒精性脂肪性肝炎的进展。在患有 NAFLD 和/或肥胖症的人类的肝脏和脂肪组织中观察到 ER 动态平衡的破坏，通常称为“ER 应激”。重要的是，破坏 ER 动态平衡激活的信号通路，未折叠蛋白反应，与脂质生物合成、胰岛素作用、炎症和细胞凋亡有关。因此，了解破坏 NAFLD 中 ER 动态平衡的机制以及 ER 介导的信号转导的作用已成为深入研究的课题。本综述将探讨 ER 和未折叠蛋白反应在 NAFLD 中的作用。
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