COX-2 in liver fibrosis

被引:73
作者
Hu Yang [1 ,2 ,3 ,4 ]
Yang Xuefeng [4 ]
Wu Shandong [5 ]
Xiao Jianhua [1 ,2 ,3 ]
机构
[1] Univ South China, Hengyang Med Coll, Inst Pathogen Biol, Hengyang 421001, Hunan, Peoples R China
[2] Hunan Prov Key Lab Special Pathogens Prevent & Co, Hengyang 421001, Hunan, Peoples R China
[3] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China
[4] Univ South China, Affiliated Nanhua Hosp, Dept Gastroenterol, Hengyang 421002, Hunan, Peoples R China
[5] Univ Alberta, Fac Sci, Dept Pharmacol, Edmonton, AB T6G 2S2, Canada
关键词
COX-2; Inflammation; Autophagy; Cell senescence; Liver fibrosis; SMOOTH-MUSCLE-CELLS; NF-KAPPA-B; CYCLOOXYGENASE-2; EXPRESSION; AUTOPHAGY ACTIVATION; CELLULAR SENESCENCE; PROSTAGLANDIN E-2; MESSENGER-RNA; INDUCTION; RECEPTOR; GROWTH;
D O I
10.1016/j.cca.2020.03.024
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
As a vital inducible sensor, cyclooxygenase-2 (COX-2) plays an important role in the progress of hepatic fibrogenesis. Activation of hepatic stellate cells (HSCs) in the liver can significantly accelerate the onset and development of liver fibrosis. COX-2 overexpression triggers inflammation that is an important inducer in hepatic fibrosis. Increasing evidence indicates that COX-2 is involved in the main pathogenesis of liver fibrosis, such as inflammation, apoptosis, and cell senescence. Moreover, COX-2 expression is altered in patients and animal models with non-alcoholic fatty liver disease or cirrhosis. These findings suggest that COX-2 has a broad and critical role in the development of liver fibrosis. In this review, we summarize the latest advances in the regulation and signal transduction of COX-2 and its impact on liver fibrosis.
引用
收藏
页码:196 / 203
页数:8
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