COX-2 in liver fibrosis

Clin Chim Acta. 2020 Jul:506:196-203. doi: 10.1016/j.cca.2020.03.024. Epub 2020 Mar 14.

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.

Keywords: Autophagy; COX-2; Cell senescence; Inflammation; Liver fibrosis.

Publication types

  • Review

MeSH terms

  • Animals
  • Cyclooxygenase 2* / genetics
  • Cyclooxygenase 2* / metabolism
  • Humans
  • Liver Cirrhosis / metabolism*
  • Signal Transduction / genetics

Substances

  • Cyclooxygenase 2