Journal
CLINICA CHIMICA ACTA
Volume 506, Issue -, Pages 196-203Publisher
ELSEVIER
DOI: 10.1016/j.cca.2020.03.024
Keywords
COX-2; Inflammation; Autophagy; Cell senescence; Liver fibrosis
Categories
Funding
- Program for Science and Technology Department of Hunan Province [2018DK51707]
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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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