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논문 기본 정보

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학술저널
저자정보
Yingzhou Shi (Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China; Key Laboratory of Endocrine Glucose) Hang Dong (Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China; Key Laboratory of Endocrine Glucose) Shiwei Sun (Key Laboratory of Endocrine Glucose) Xiaoqin Wu (Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, USA) Jiansong Fang (Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China) Jianbo Zhao (Key Laboratory of Endocrine Glucose) Junming Han (Key Laboratory of Endocrine Glucose) Zongyue Li (Key Laboratory of Endocrine Glucose) Huixiao Wu (Key Laboratory of Endocrine Glucose) Luna Liu (Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China; Key Laboratory of Endocrine Glucose) Wanhong Wu (Key Laboratory of Endocrine Glucose) Yang Tian (Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China; Key Laboratory of Endocrine Glucose) Guandou Yuan (Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China) Xiude Fan (Key Laboratory of Endocrine Glucose) Chao Xu (Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China; Key Laboratory of Endocrine Glucose)
저널정보
대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology Vol.30 No.1
발행연도
2024.1
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80 - 97 (18page)

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Background/Aims: To evaluate the causal correlation between complement components and non-viral liver diseases and their potential use as druggable targets. Methods: We conducted Mendelian randomization (MR) to assess the causal role of circulating complements in the risk of non-viral liver diseases. A complement-centric protein interaction network was constructed to explore biological functions and identify potential therapeutic options. Results: In the MR analysis, genetically predicted levels of complement C1q C chain (C1QC) were positively associated with the risk of autoimmune hepatitis (odds ratio 1.125, 95% confidence interval 1.018–1.244), while complement factor H-related protein 5 (CFHR5) was positively associated with the risk of primary sclerosing cholangitis (PSC;1.193, 1.048– 1.357). On the other hand, CFHR1 (0.621, 0.497–0.776) and CFHR2 (0.824, 0.703–0.965) were inversely associated with the risk of alcohol-related cirrhosis. There were also significant inverse associations between C8 gamma chain (C8G) and PSC (0.832, 0.707–0.979), as well as the risk of metabolic dysfunction-associated steatotic liver disease (1.167, 1.036–1.314). Additionally, C1S (0.111, 0.018–0.672), C7 (1.631, 1.190–2.236), and CFHR2 (1.279, 1.059–1.546) were significantly associated with the risk of hepatocellular carcinoma. Proteins from the complement regulatory networks and various liver diseaserelated proteins share common biological processes. Furthermore, potential therapeutic drugs for various liver diseases were identified through drug repurposing based on the complement regulatory network. Conclusions: Our study suggests that certain complement components, including C1S, C1QC, CFHR1, CFHR2, CFHR5, C7, and C8G, might play a role in non-viral liver diseases and could be potential targets for drug development.
#Liver diseases #Complement system proteins #Mendelian randomization analysis #Drug repositioning

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