The role of complement in nonalcoholic fatty liver disease

被引:26
作者
Guo, Zhenya [1 ,2 ,3 ]
Fan, Xiude [4 ]
Yao, Jianni [2 ,3 ]
Tomlinson, Stephen [5 ]
Yuan, Guandou [1 ,2 ,3 ]
He, Songqing [1 ,2 ,3 ]
机构
[1] Guangxi Med Univ, Affiliated Hosp 1, Div Hepatobiliary Surg, Nanning, Peoples R China
[2] Guangxi Med Univ, Key Lab Early Prevent & Treatment Reg High Frequen, Minist Educ, Nanning, Peoples R China
[3] Guangxi Med Univ, Guangxi Key Lab Immunol & Metab Liver Dis, Nanning, Peoples R China
[4] Shandong First Med Univ, Shandong Prov Hosp, Dept Endocrinol, Jinan, Peoples R China
[5] Med Univ South Carolina, Dept Microbiol & Immunol, Charleston, SC USA
基金
中国国家自然科学基金;
关键词
complement system; nonalcoholic fatty liver disease; site-targeted inhibitor; inflammation; liver; ADIPOSE-TISSUE; INSULIN-RESISTANCE; TICK-OVER; T-CELLS; INFLAMMATION; ACTIVATION; C3A; STEATOHEPATITIS; RECEPTOR; PATHOGENESIS;
D O I
10.3389/fimmu.2022.1017467
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Nonalcoholic fatty liver disease (NAFLD) has become a leading cause of chronic liver diseases globally. NAFLD includes a range of hepatic manifestations, starting with liver steatosis and potentially evolving towards nonalcoholic steatohepatitis, cirrhosis or even hepatocellular carcinoma. Although the pathogenesis of NAFLD is incompletely understood, insulin resistance and lipid metabolism disorder are implicated. The complement system is an essential part of the immune system, but it is also involved in lipid metabolism. In particular, activation of the alternative complement pathway and the production of complement activation products such as C3a, C3adesArg (acylation stimulating protein or ASP) and C5a, are strongly associated with insulin resistance, lipid metabolism disorder, and hepatic inflammation. In this review, we briefly summarize research on the role of the complement system in NAFLD, aiming to provide a basis for the development of novel therapeutic strategies for NAFLD.
引用
收藏
页数:9
相关论文
共 84 条
[11]  
CIANFLONE K, 1995, INT J OBESITY, V19, P604
[12]   ADIPSIN - A CIRCULATING SERINE PROTEASE HOMOLOG SECRETED BY ADIPOSE-TISSUE AND SCIATIC-NERVE [J].
COOK, KS ;
MIN, HY ;
JOHNSON, D ;
CHAPLINSKY, RJ ;
FLIER, JS ;
HUNT, CR ;
SPIEGELMAN, BM .
SCIENCE, 1987, 237 (4813) :402-405
[13]   Nonalcoholic Fatty Liver Disease 2020: The State of the Disease [J].
Cotter, Thomas G. ;
Rinella, Mary .
GASTROENTEROLOGY, 2020, 158 (07) :1851-1864
[14]   Is the Complement Activation Product C3a a Proinflammatory Molecule? Re-evaluating the Evidence and the Myth [J].
Coulthard, Liam G. ;
Woodruff, Trent M. .
JOURNAL OF IMMUNOLOGY, 2015, 194 (08) :3542-3548
[15]  
Dudek M, 2021, J HEPATOL, V75, pS262
[16]   Complement Factor C5a Inhibits Apoptosis of Neutrophils-A Mechanism in Polytrauma? [J].
Ehrnthaller, Christian ;
Braumueller, Sonja ;
Kellermann, Stephanie ;
Gebhard, Florian ;
Perl, Mario ;
Huber-Lang, Markus .
JOURNAL OF CLINICAL MEDICINE, 2021, 10 (14)
[17]   Inflammation and fibrogenesis in steatohepatitis [J].
Fujii, Hideki ;
Kawada, Norifumi .
JOURNAL OF GASTROENTEROLOGY, 2012, 47 (03) :215-225
[18]   Chylomicron accelerates C3 tick-over by regulating the role of factor H, leading to overproduction of acylation stimulating protein [J].
Fujita, Takayuki ;
Fujioka, Takayuki ;
Murakami, Tetsuo ;
Satomura, Atsushi ;
Fuke, Yoshinobu ;
Matsumoto, Koichi .
JOURNAL OF CLINICAL LABORATORY ANALYSIS, 2007, 21 (01) :14-23
[19]   High expression of complement components in omental adipose tissue in obese men [J].
Gabrielsson, BG ;
Johansson, JM ;
Lönn, M ;
Jernås, M ;
Olbers, T ;
Peltonen, M ;
Larsson, I ;
Lönn, L ;
Sjöström, L ;
Carlsson, B ;
Carlsson, LMS .
OBESITY RESEARCH, 2003, 11 (06) :699-708
[20]   IL-17 Axis Driven Inflammation in Non-Alcoholic Fatty Liver Disease Progression [J].
Giles, Daniel A. ;
Moreno-Fernandez, Maria E. ;
Divanovic, Senad .
CURRENT DRUG TARGETS, 2015, 16 (12) :1315-1323