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.

中文翻译：

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肝纤维化中的COX-2。

作为重要的诱导型传感器，环氧合酶2（COX-2）在肝纤维化进程中起着重要作用。肝中肝星状细胞（HSC）的激活可以显着加速肝纤维化的发生和发展。COX-2的过表达引发炎症，这是肝纤维化的重要诱因。越来越多的证据表明，COX-2参与了肝纤维化的主要发病机制，例如炎症，细胞凋亡和细胞衰老。而且，在患有非酒精性脂肪肝或肝硬化的患者和动物模型中，COX-2的表达发生了改变。这些发现表明，COX-2在肝纤维化的发展中具有广泛而关键的作用。在这篇综述中，我们总结了COX-2的调控和信号转导及其对肝纤维化的影响的最新进展。