Regulation of necroptosis signaling and cell death by reactive oxygen species

被引：81

作者：

Fulda, Simone ^{[1
,2
,3
]}

机构：

[1] Goethe Univ Frankfurt, Inst Expt Canc Res Pediat, Komturstr 3a, D-60528 Frankfurt, Germany

[2] German Canc Consortium DKTK, D-69120 Heidelberg, Germany

[3] German Canc Res Ctr, D-69120 Heidelberg, Germany

来源：

BIOLOGICAL CHEMISTRY | 2016年 / 397卷 / 07期

关键词：

cell death; necroptosis; ROS; MITOCHONDRIAL PERMEABILITY TRANSITION; TNF-INDUCED NECROSIS; ALPHA;

D O I：

10.1515/hsz-2016-0102

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Necroptosis has recently been identified as an alternative form of programmed cell death that is characterized by defined molecular mechanisms. Reactive oxygen species (ROS) are involved in the regulation of numerous signaling pathways, as they are highly reactive and can cause (ir)reversible posttranslational modifications. While the role of ROS in other modes of cell death has been extensively studied, its impact on necroptotic signaling and cell death is far less clear. The current mini-review discusses the evidence for and against a role of ROS in necroptosis.

引用

页码：657 / 660

页数：4

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