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Published on: February 10, 2015
COX-2 in liver fibrosis
Hu Yang1, Yang Xuefeng2, Wu Shandong3
1Institute of Pathogenic Biology, Hengyang Medical College, University of South China, Hengyang 421001, Hunan, China; Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hengyang 421001, Hunan, China; Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, Hunan, China; Department of Gastroenterology, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, China.
Abstract:
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.
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