Suppr超能文献

COX-2 在肝纤维化中的作用。

COX-2 in liver fibrosis.

机构信息

Institute 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.

Department of Gastroenterology, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, China.

出版信息

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.

摘要

作为一种重要的诱导型传感器,环氧合酶-2(COX-2)在肝纤维化的进展中起着重要作用。肝脏中肝星状细胞(HSCs)的激活可显著加速肝纤维化的发生和发展。COX-2 的过度表达引发炎症,这是肝纤维化的重要诱导因素。越来越多的证据表明,COX-2 参与肝纤维化的主要发病机制,如炎症、细胞凋亡和细胞衰老。此外,非酒精性脂肪性肝病或肝硬化患者和动物模型中 COX-2 的表达发生改变。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 的调节和信号转导及其对肝纤维化影响的最新进展。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验