Molecular mechanisms of necroptosis: an ordered cellular explosion

被引：1854

作者：

Vandenabeele, Peter ^{[1
,2
]}

Galluzzi, Lorenzo ^{[3
,4
,5
]}

Vanden Berghe, Tom ^{[1
,2
]}

Kroemer, Guido ^{[3
,4
,6
,7
,8
]}

机构：

[1] Univ Ghent VIB, Mol Signalling & Cell Death Unit, Dept Mol Biomed Res, B-9052 Ghent, Belgium

[2] Univ Ghent VIB, Dept Biomed Mol Biol, B-9052 Ghent, Belgium

[3] INSERM, U848, F-94805 Villejuif, France

[4] Inst Gustave Roussy, F-94805 Villejuif, France

[5] Univ Paris 11, F-94805 Villejuif, France

[6] Ctr Rech Cordoliers, F-75005 Paris, France

[7] Pole Biol Hop Europeen Georges Pompidou, AP HP, F-75908 Paris, France

[8] Univ Paris 05, F-75270 Paris, France

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2010年 / 11卷 / 10期

关键词：

TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; RECEPTOR-INTERACTING PROTEIN; MITOCHONDRIAL PERMEABILITY TRANSITION; APOPTOSIS-INDUCING FACTOR; LYSOSOMAL MEMBRANE PERMEABILIZATION; MEDIATED PROGRAMMED NECROSIS; FOCAL CEREBRAL-ISCHEMIA; DEATH DOMAIN KINASE; OXIDATIVE STRESS;

D O I：

10.1038/nrm2970

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

For a long time, apoptosis was considered the sole form of programmed cell death during development, homeostasis and disease, whereas necrosis was regarded as an unregulated and uncontrollable process. Evidence now reveals that necrosis can also occur in a regulated manner. The initiation of programmed necrosis, 'necroptosis', by death receptors (such as tumour necrosis factor receptor 1) requires the kinase activity of receptor-interacting protein 1 (RIP1; also known as RIPK1) and RIP3 (also known as RIPK3), and its execution involves the active disintegration of mitochondrial, lysosomal and plasma membranes. Necroptosis participates in the pathogenesis of diseases, including ischaemic injury, neurodegeneration and viral infection, thereby representing an attractive target for the avoidance of unwarranted cell death.

引用

页码：700 / 714

页数：15

共 171 条

[1] Poly(ADP-ribose) polymerase-1-mediated cell death in astrocytes requires NAD+ depletion and mitochondrial permeability transition [J].