Necroptosis: An emerging form of programmed cell death

被引：198
作者：
Wu, Wei [1 ]
Liu, Peng [1 ]
Li, Jianyong [1 ]
机构：
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Hematol, Nanjing 210029, Jiangsu, Peoples R China
来源：
CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY | 2012年 / 82卷 / 03期
基金：
中国国家自然科学基金;
关键词：
Necroptosis; Apoptosis; Cell death; Cancer; TUMOR-NECROSIS-FACTOR; RECEPTOR-INTERACTING PROTEIN; MITOCHONDRIAL PERMEABILITY TRANSITION; CYTOSOLIC PHOSPHOLIPASE A(2); KAPPA-B ACTIVATION; NITRIC-OXIDE; CYCLOPHILIN-D; FACTOR-ALPHA; NADPH OXIDASE; RIP KINASES;
D O I：
10.1016/j.critrevonc.2011.08.004
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Necrosis plays an important role in multiple physiological and pathological processes. Recently, a relatively new form of necrosis has been characterized as "necroptosis". Morphologically, necroptosis exhibits the features of necrosis; however, necroptosis exhibits a unique signaling pathway that requires the involvement of receptor interaction protein kinase 1 and 3 (RIP1 and RIP3) and can be specifically inhibited by necrostatins. Necroptosis has been found to contribute to the regulation of immune system, cancer development as well as cellular responses to multiple stresses. In this review, we will summarize the signaling pathway, biological effects and pathological significance of this specific form of programmed cell death. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：249 / 258
页数：10
相关论文
共 120 条
  • [51] Activation of death-inducing signaling complex (DISC) by pro-apoptotic C-terminal fragment of RIP
    Kim, JW
    Choi, EJ
    Joe, CO
    [J]. ONCOGENE, 2000, 19 (39) : 4491 - 4499
  • [52] TNF-induced activation of the Nox1 NADPH oxidase and its role in the induction of necrotic cell death
    Kim, You-Sun
    Morgan, Michael J.
    Choksi, Swati
    Liu, Zheng-Gang
    [J]. MOLECULAR CELL, 2007, 26 (05) : 675 - 687
  • [53] Role of phospholipase A2 in the cytotoxic effects of oxalate in cultured renal epithelial cells
    Kohjimoto, Y
    Kennington, L
    Scheid, CR
    Honeyman, TW
    [J]. KIDNEY INTERNATIONAL, 1999, 56 (04) : 1432 - 1441
  • [54] The tumour suppressor CYLD negatively regulates NF-κB signalling by deubiquitination
    Kovalenko, A
    Chable-Bessia, C
    Cantarella, G
    Israël, A
    Wallach, D
    Courtois, G
    [J]. NATURE, 2003, 424 (6950) : 801 - 805
  • [55] Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009
    Kroemer, G.
    Galluzzi, L.
    Vandenabeele, P.
    Abrams, J.
    Alnemri, E. S.
    Baehrecke, E. H.
    Blagosklonny, M. V.
    El-Deiry, W. S.
    Golstein, P.
    Green, D. R.
    Hengartner, M.
    Knight, R. A.
    Kumar, S.
    Lipton, S. A.
    Malorni, W.
    Nunez, G.
    Peter, M. E.
    Tschopp, J.
    Yuan, J.
    Piacentini, M.
    Zhivotovsky, B.
    Melino, G.
    [J]. CELL DEATH AND DIFFERENTIATION, 2009, 16 (01) : 3 - 11
  • [56] Nox enzymes and the biology of reactive oxygen
    Lambeth, JD
    [J]. NATURE REVIEWS IMMUNOLOGY, 2004, 4 (03) : 181 - 189
  • [57] LASTER SM, 1988, J IMMUNOL, V141, P2629
  • [58] TRAF2 is essential for JNK but not NF-kappa B activation and regulates lymphocyte proliferation and survival
    Lee, SY
    Reichlin, A
    Santana, A
    Sokol, KA
    Nussenzweig, MC
    Choi, Y
    [J]. IMMUNITY, 1997, 7 (05) : 703 - 713
  • [59] The kinase activity of Rip1 is not required for tumor necrosis factor-α-induced IκB kinase or p38 MAP kinase activation or for the ubiquitination of Rip1 by Traf2
    Lee, TH
    Shank, J
    Cusson, N
    Kelliher, MA
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (32) : 33185 - 33191
  • [60] NOX3-derived reactive oxygen species promote TNF-α-induced reductions in hepatocyte glycogen levels via a JNK pathway
    Li, Lanfang
    He, Qinghua
    Huang, Xiuqing
    Man, Yong
    Zhou, Yingsheng
    Wang, Shu
    Wang, Jianye
    Li, Jian
    [J]. FEBS LETTERS, 2010, 584 (05): : 995 - 1000
12345678910