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补体成分C3:一种参与非酒精性脂肪性肝病发病机制的新型生物标志物。

Complement Component C3: A Novel Biomarker Participating in the Pathogenesis of Non-alcoholic Fatty Liver Disease.

作者信息

Han Juqiang, Zhang Xiang

机构信息

Institute of Liver Disease, The 7th Medical Centre of Chinese People Liberation Army General Hospital, Beijing, China.

The Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease, Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China.

出版信息

Front Med (Lausanne). 2021 Jul 29;8:653293. doi: 10.3389/fmed.2021.653293. eCollection 2021.

DOI:10.3389/fmed.2021.653293
PMID:34395461
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8358116/
Abstract

Non-alcoholic fatty liver disease (NAFLD) is currently the most common cause of chronic liver disorder worldwide. The pathological spectrum of NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH) that induces progressive liver cirrhosis and eventually hepatocellular carcinoma (HCC). However, the molecular mechanisms driving the transformation of NASH are obscure. There is a compelling need for understanding the pathogenic mechanisms of NASH, and thereby providing new insight into mechanism-based therapy. Currently, several studies reported that complement system, an innate immune system, played an important role in the pathogenesis of NAFLD, which was also proved by our recent study. Complement component 3 (C3), a protein of the innate immune system, plays a hub role in the complement system. Herein, we present a review on the role and molecular mechanism of C3 in NASH as well as its implication in NASH diagnosis and treatment.

摘要

非酒精性脂肪性肝病(NAFLD)是目前全球慢性肝脏疾病最常见的病因。NAFLD的病理谱范围从单纯性脂肪变性到非酒精性脂肪性肝炎(NASH),后者可导致进行性肝硬化并最终发展为肝细胞癌(HCC)。然而,驱动NASH转变的分子机制尚不清楚。迫切需要了解NASH的致病机制,从而为基于机制的治疗提供新的见解。目前,多项研究报道补体系统作为一种固有免疫系统,在NAFLD的发病机制中起重要作用,我们最近的研究也证实了这一点。补体成分3(C3)作为固有免疫系统的一种蛋白质,在补体系统中起核心作用。在此,我们综述C3在NASH中的作用和分子机制及其在NASH诊断和治疗中的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/1e4e60bf3e88/fmed-08-653293-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/15aa74451523/fmed-08-653293-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/9b0edbed052a/fmed-08-653293-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/1e4e60bf3e88/fmed-08-653293-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/15aa74451523/fmed-08-653293-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/9b0edbed052a/fmed-08-653293-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea4e/8358116/1e4e60bf3e88/fmed-08-653293-g0003.jpg

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