线粒体通透性转换孔
自噬
程序性细胞死亡
线粒体
细胞凋亡
脂肪变性
胆汁淤积
细胞生物学
肝损伤
肝细胞
药品
坏死
受体
生物
癌症研究
药理学
医学
病理
体外
内分泌学
生物化学
标识
DOI:10.1016/j.cbi.2006.06.007
摘要
Hepatic injury remains not only the commonest reason for the termination of drugs in their pre-clinical development but is also the most frequent reason for the withdrawal of approved drugs from the market. Mitochondria are the central point where the different signals responsible for initiating hepatocyte cell death converge, irrespective of whether the cells ultimately die by apoptosis, necrosis (oncosis) or autophagic cell death. These signals can be in the form of direct damage to the mitochondria leading to permeability transition or can act indirectly through activation of death receptors and downstream pro-apoptotic Bcl-2 family proteins. This paper reviews our current knowledge about how hepatotoxic drugs, whether direct acting or through induction of steatosis or cholestasis, target mitochondria and cause hepatic injury.
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