Necrotic death as a cell fate

被引:681
作者
Zong, WX
Thompson, CB [1 ]
机构
[1] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
[2] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA
关键词
ROS; calcium; mitochondria; necrosis;
D O I
10.1101/gad.1376506
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Organismal homeostasis depends on an intricate balance between cell death and renewal. Early pathologists recognized that this balance could be disrupted by the extensive damage observed in internal organs during the course of certain diseases. This form of tissue damage was termed "necrosis", derived from the Greek "nekros" for corpse. As it became clear that the essential building block of tissue was the cell, necrosis came to be used to describe pathologic cell death. Until recently, necrotic cell death was believed to result from injuries that caused an irreversible bioenergetic compromise. The cell dying by necrosis has been viewed as a victim of extrinsic events beyond its control. However, recent evidence suggests that a cell can initiate its own demise by necrosis in a manner that initiates both inflammatory and/or reparative responses in the host. By initiating these adaptive responses, programmed cell necrosis may serve to maintain tissue and organismal integrity.
引用
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页码:1 / 15
页数:15
相关论文
共 171 条
  • [1] A key role for TRPM7 channels in anoxic neuronal death
    Aarts, M
    Iihara, K
    Wei, WL
    Xiong, ZG
    Arundine, M
    Cerwinski, W
    MacDonald, JF
    Tymianski, M
    [J]. CELL, 2003, 115 (07) : 863 - 877
  • [2] Regulatory pathways in photodynamic therapy induced apoptosis
    Agostinis, P
    Buytaert, E
    Breyssens, H
    Hendrickx, N
    [J]. PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES, 2004, 3 (08) : 721 - 729
  • [3] Intracellular signaling mechanisms in photodynamic therapy
    Almeida, RD
    Manadas, BJ
    Carvalho, AP
    Duarte, CB
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 2004, 1704 (02): : 59 - 86
  • [4] Mitochondrial metabolism of reactive oxygen species
    Andreyev, AI
    Kushnareva, YE
    Starkov, AA
    [J]. BIOCHEMISTRY-MOSCOW, 2005, 70 (02) : 200 - 214
  • [5] GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION
    ANKARCRONA, M
    DYPBUKT, JM
    BONFOCO, E
    ZHIVOTOVSKY, B
    ORRENIUS, S
    LIPTON, SA
    NICOTERA, P
    [J]. NEURON, 1995, 15 (04) : 961 - 973
  • [6] DEVIANT ENERGETIC METABOLISM OF GLYCOLYTIC CANCER-CELLS
    BAGGETTO, LG
    [J]. BIOCHIMIE, 1992, 74 (11) : 959 - 974
  • [7] Honokiol, a small molecular weight natural product, inhibits angiogenesis in vitro and tumor growth in vivo
    Bai, XH
    Cerimele, F
    Ushio-Fukai, M
    Waqas, M
    Campbell, PM
    Govindarajan, B
    Der, CJ
    Battle, T
    Frank, DA
    Ye, KQ
    Murad, E
    Dubiel, W
    Soff, G
    Arbiser, JL
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (37) : 35501 - 35507
  • [8] Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
    Baines, CP
    Kaiser, RA
    Purcell, NH
    Blair, NS
    Osinska, H
    Hambleton, MA
    Brunskill, EW
    Sayen, MR
    Gottlieb, RA
    Dorn, GW
    Robbins, J
    Molkentin, JD
    [J]. NATURE, 2005, 434 (7033) : 658 - 662
  • [9] Cleavage of the plasma membrane Na+/Ca2+ exchanger in excitotoxicity
    Bano, D
    Young, KW
    Guerin, CJ
    LeFeuvre, R
    Rothwell, NJ
    Naldini, L
    Rizzuto, R
    Carafoli, E
    Nicotera, P
    [J]. CELL, 2005, 120 (02) : 275 - 285
  • [10] Barger AJ, 1998, J NEUROSCI, V18, P2871