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肝脏再生增强因子在非酒精性脂肪性肝病中对肝细胞的保护作用。

The protective roles of augmenter of liver regeneration in hepatocytes in the non-alcoholic fatty liver disease.

作者信息

Dong Yuan, Zhang Yuejie, Feng Yingmei, An Wei

机构信息

Department of Science and Technology, Beijing Youan Hospital, Capital Medical University, Beijing, China.

Department of Cell Biology, Capital Medical University and the Municipal Key Laboratory for Liver Protection and Regulation of Regeneration, Beijing, China.

出版信息

Front Pharmacol. 2022 Oct 11;13:928606. doi: 10.3389/fphar.2022.928606. eCollection 2022.

Abstract

Non-alcoholic fatty liver disease (NAFLD) occurs in 25% of the global population and manifests as lipid deposition, hepatocyte injury, activation of Kupffer and stellate cells, and steatohepatitis. Predominantly expressed in hepatocytes, the augmenter of liver regeneration (ALR) is a key factor in liver regulation that can alleviate fatty liver disease and protect the liver from abnormal liver lipid metabolism. ALR has three isoforms (15-, 21-, and 23-kDa), amongst which 23-kDa ALR is the most extensively studied. The 23-kDa ALR isoform is a sulfhydryl oxidase that resides primarily in the mitochondrial intermembrane space (IMS), whereby it protects the liver against various types of injury. In this review, we describe the role of ALR in regulating hepatocytes in the context of NAFLD. We also discuss questions about ALR that remain to be explored in the future. In conclusion, ALR appears to be a promising therapeutic target for treating NAFLD.

摘要

非酒精性脂肪性肝病(NAFLD)在全球25%的人口中出现,表现为脂质沉积、肝细胞损伤、库普弗细胞和星状细胞活化以及脂肪性肝炎。肝脏再生增强因子(ALR)主要在肝细胞中表达,是肝脏调节的关键因子,可减轻脂肪肝疾病并保护肝脏免受异常肝脏脂质代谢的影响。ALR有三种同工型(15 kDa、21 kDa和23 kDa),其中23 kDa的ALR研究最为广泛。23 kDa的ALR同工型是一种巯基氧化酶,主要存在于线粒体内膜间隙(IMS)中,从而保护肝脏免受各种类型的损伤。在这篇综述中,我们描述了ALR在NAFLD背景下调节肝细胞的作用。我们还讨论了关于ALR未来仍有待探索的问题。总之,ALR似乎是治疗NAFLD的一个有前景的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec32/9592723/61d126a76aae/fphar-13-928606-g001.jpg

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