摘要
非酒精性脂肪性肝病(NAFLD)是一种常见的公共卫生问题,被认为是肝病的主要驱动因素。然而,触发NAFLD发展的基本机制仍然有些难以捉摸。内质网(ER)应激促进未折叠蛋白反应(UPR),并导致脂肪变性,非酒精性脂肪性肝炎和最终肝癌的病因学。虽然ER应激可能导致一系列补偿性反应,有助于恢复ER稳态,细胞存活和适应,但已知延长的ER应激会产生有害的病理结果,包括胰岛素抵抗,异位脂肪沉积,炎症,细胞凋亡和失调的自噬。所有这些过程都能够激发NAFLD的发生和发展。为此,了解ER应激在NAFLD的发生和发展中对于这种破坏性代谢疾病的正确管理的作用是恰当的。在本综述中,我们将总结有关ER应激在NAFLD病因学中潜在作用的最新进展的可用信息
关键词: ER应激,肝脏,非酒精性脂肪肝病,代谢性疾病,未折叠蛋白反应,自噬。
图形摘要
Current Drug Targets
Title:Endoplasmic Reticulum Stress Related Molecular Mechanisms in Nonalcoholic Fatty Liver Disease (NAFLD)
Volume: 19 Issue: 9
关键词: ER应激,肝脏,非酒精性脂肪肝病,代谢性疾病,未折叠蛋白反应,自噬。
摘要: Non-alcoholic fatty liver disease (NAFLD) is a common public health issue and is considered a main drive for liver diseases. However, the basic mechanisms that trigger the development of NAFLD still remain somewhat elusive. Endoplasmic reticulum (ER) stress facilitates the unfolded protein response (UPR) and contributes to the etiology of steatosis, nonalcoholic steatohepatitis and ultimately hepatocarcinoma. Although ER stress may lead to a cascade of compensatory responses that help to restore ER homeostasis, cell survival and adaptation, prolonged ER stress is known to impose detrimental pathological outcome, involving insulin resistance, ectopic fat deposition, inflammation, apoptosis, and dysregulated autophagy. All of these processes are capable of provoking the onset and development of NAFLD. To this end, it is pertinent to understand the role of ER stress in the onset and progression of NAFLD for proper management of this devastating metabolic disease. Here in this review, we will summarize available information on the recent advances in the potential role for ER stress in the etiology of NAFLD.
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Cite this article as:
Endoplasmic Reticulum Stress Related Molecular Mechanisms in Nonalcoholic Fatty Liver Disease (NAFLD), Current Drug Targets 2018; 19 (9) . https://dx.doi.org/10.2174/1389450118666180516122517
DOI https://dx.doi.org/10.2174/1389450118666180516122517 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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