内质网
利福平
孕烷X受体
氧化应激
未折叠蛋白反应
药理学
肝损伤
毒性
细胞色素P450
化学
生物
医学
细胞生物学
微生物学
内科学
内分泌学
生物化学
酶
核受体
抗生素
基因
转录因子
作者
Wanqing Hou,Bernard Nsengimana,Chuyun Yan,Bjorn Nashan,Seung Yun Han
标识
DOI:10.3389/fphar.2022.1022809
摘要
Rifampicin is a first-line antituberculosis drug. Hepatocyte toxicity caused by rifampicin is a significant clinical problem. However, the specific mechanism by which rifampicin causes liver injury is still poorly understood. Endoplasmic reticulum (ER) stress can have both protective and proapoptotic effects on an organism, depending on the environmental state of the organism. While causing cholestasis and oxidative stress in the liver, rifampicin also activates ER stress in different ways, including bile acid accumulation and cytochrome p450 (CYP) enzyme-induced toxic drug metabolites via pregnane X receptor (PXR). The short-term stress response helps the organism resist toxicity, but when persisting, the response aggravates liver damage. Therefore, ER stress may be closely related to the “adaptive” mechanism and the apoptotic toxicity of rifampicin. This article reviews the functional characteristics of ER stress and its potentially pathogenic role in liver injury caused by rifampicin.
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