Zhang Xue-Qun, Xu Cheng-Fu, Yu Chao-Hui, Chen Wei-Xing, Li You-Ming
Xue-Qun Zhang, Cheng-Fu Xu, Chao-Hui Yu, Wei-Xing Chen, You-Ming Li, Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China.
World J Gastroenterol. 2014 Feb 21;20(7):1768-76. doi: 10.3748/wjg.v20.i7.1768.
Nonalcoholic fatty liver disease (NAFLD) has emerged as a common public health problem in recent decades. However, the underlying mechanisms leading to the development of NAFLD are not fully understood. The endoplasmic reticulum (ER) stress response has recently been proposed to play a crucial role in both the development of steatosis and progression to nonalcoholic steatohepatitis. ER stress is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed due to the accumulation of unfolded or misfolded proteins. However, delayed or insufficient responses to ER stress may turn physiological mechanisms into pathological consequences, including fat accumulation, insulin resistance, inflammation, and apoptosis, all of which play important roles in the pathogenesis of NAFLD. Therefore, understanding the role of ER stress in the pathogenesis of NAFLD has become a topic of intense investigation. This review highlights the recent findings linking ER stress signaling pathways to the pathogenesis of NAFLD.
近几十年来，非酒精性脂肪性肝病（NAFLD）已成为一个常见的公共卫生问题。然而，导致NAFLD发生发展的潜在机制尚未完全明确。最近有研究提出，内质网（ER）应激反应在脂肪变性的发展以及向非酒精性脂肪性肝炎的进展过程中均起着关键作用。当细胞因未折叠或错误折叠蛋白质的积累而受到应激时，内质网应激被激活以调节蛋白质合成并恢复稳态平衡。然而，对内质网应激的延迟或不足反应可能会使生理机制转变为病理后果，包括脂肪堆积、胰岛素抵抗、炎症和细胞凋亡，所有这些在NAFLD的发病机制中都起着重要作用。因此，了解内质网应激在NAFLD发病机制中的作用已成为一个深入研究的课题。本综述重点介绍了将内质网应激信号通路与NAFLD发病机制联系起来的最新研究发现。
