Molecular mechanisms of hepatic apoptosis

被引:250
作者
Wang, K. [1 ]
机构
[1] Univ Illinois, Coll Med Peoria, Dept Surg, Peoria, IL 61605 USA
关键词
hepatic apoptosis; liver injury; ROS; ER stress; lysosomal permeabilization; mitochondrial dysfunction; INDUCED LIVER-INJURY; CYTOKINE GENE POLYMORPHISM; HCV STRUCTURAL PROTEINS; TRAIL-INDUCED APOPTOSIS; PROGRAMMED CELL-DEATH; C VIRUS-INFECTION; FATTY LIVER; HEPATOCYTE APOPTOSIS; MEDIATED-APOPTOSIS; URSODEOXYCHOLIC ACID;
D O I
10.1038/cddis.2013.499
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Apoptosis is a prominent feature of liver diseases. Causative factors such as alcohol, viruses, toxic bile acids, fatty acids, drugs, and immune response, can induce apoptotic cell death via membrane receptors and intracellular stress. Apoptotic signaling network, including membrane death receptor-mediated cascade, reactive oxygen species (ROS) generation, endoplasmic reticulum (ER) stress, lysosomal permeabilization, and mitochondrial dysfunction, is intermixed each other, but one mechanism may dominate at a particular stage. Mechanisms of hepatic apoptosis are complicated by multiple signaling pathways. The progression of liver disease is affected by the balance between apoptotic and antiapoptotic capabilities. Therapeutic options of liver injury are impacted by the clear understanding toward mechanisms of hepatic apoptosis.
引用
收藏
页码:e996 / e996
页数:10
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