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酒精与肝纤维化

Alcohol and liver fibrosis.

作者信息

Cubero Francisco Javier, Urtasun Raquel, Nieto Natalia

机构信息

Department of Medicine, Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA.

出版信息

Semin Liver Dis. 2009 May;29(2):211-21. doi: 10.1055/s-0029-1214376. Epub 2009 Apr 22.

Abstract

Alcoholic liver disease involves significant crosstalk among intracellular signaling events in the liver. Overall, inflammatory and innate immune responses in Kupffer cells due to elevated gut-derived plasma endotoxin levels, increased reactive oxygen species-induced damage, and profibrogenic factors such as acetaldehyde or lipid peroxidation products contribute to activation of hepatic stellate cells, the key cell type involved in liver fibrosis. Using in vitro and in vivo approaches, there has been great progress in our understanding of the mechanisms leading to liver fibrosis: potential biomarkers of fibrosis have been identified, and several candidate targets for antifibrotic drugs have been elucidated.

摘要

酒精性肝病涉及肝脏细胞内信号事件之间的显著相互作用。总体而言,由于肠道来源的血浆内毒素水平升高、活性氧诱导的损伤增加以及乙醛或脂质过氧化产物等促纤维化因子,库普弗细胞中的炎症和先天性免疫反应导致肝星状细胞激活,肝星状细胞是参与肝纤维化的关键细胞类型。通过体外和体内研究方法,我们对导致肝纤维化的机制有了很大进展:已确定了潜在的纤维化生物标志物,并阐明了几种抗纤维化药物的候选靶点。

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