Programmed Necrosis: A “New” Cell Death Outcome for Injured Adult Neurons?

作者: Slavica Krantic , Santos A. Susin

DOI: 10.1007/978-0-387-73226-8_3

关键词:

摘要: Historically, cell death has been divided into two generic categories: apoptosis, which requires energy and in the plays an active role, necrosis, occurs accidentally, does not require consumption is considered as a passive, uncontrolled program. Among conceptually opposite forms, apoptosis best understood. This program defined developmentally programmed ordered cellular response. Apoptosis initiated by rounding subsequent detachment from surrounding cells. Chromatin condenses “crescent-like” forms abutting inner nuclear membrane. Plasma membrane convolutes gives rise to characteristic vesicles containing organelles cytoplasm, known “apoptotic bodies.” generally accompanied inflammation since macrophages or neighbouring cells engulf formed apoptotic bodies before loss of plasma integrity (Kerr et al. 1972). In contrast necrosis characterized disruption with water influx leakage content surroundings. Cell can elicit inflammatory response (Edinger Thompson 2004).

参考文章(204)
Marja Jäättelä, Jürg Tschopp, Caspase-independent cell death in T lymphocytes Nature Immunology. ,vol. 4, pp. 416- 423 ,(2003) , 10.1038/NI0503-416
Rana S. Moubarak, Victor J. Yuste, Cédric Artus, Aïda Bouharrour, Peter A. Greer, Josiane Menissier-de Murcia, Santos A. Susin, Sequential Activation of Poly(ADP-Ribose) Polymerase 1, Calpains, and Bax Is Essential in Apoptosis-Inducing Factor-Mediated Programmed Necrosis Molecular and Cellular Biology. ,vol. 27, pp. 4844- 4862 ,(2007) , 10.1128/MCB.02141-06
Cheikh I Seye, Michiel WM Knaapen, Danièle Daret, Claude Desgranges, Arnold G Herman, Mark M Kockx, Hidde Bult, 7-Ketocholesterol induces reversible cytochrome c release in smooth muscle cells in absence of mitochondrial swelling. Cardiovascular Research. ,vol. 64, pp. 144- 153 ,(2004) , 10.1016/J.CARDIORES.2004.05.016
R V Rao, H M Ellerby, D E Bredesen, Coupling endoplasmic reticulum stress to the cell death program. Cell Death & Differentiation. ,vol. 11, pp. 372- 380 ,(2004) , 10.1038/SJ.CDD.4401378
G. Cao, J. Xing, X. Xiao, A. K. F. Liou, Y. Gao, X.-M. Yin, R. S. B. Clark, S. H. Graham, J. Chen, Critical Role of Calpain I in Mitochondrial Release of Apoptosis-Inducing Factor in Ischemic Neuronal Injury The Journal of Neuroscience. ,vol. 27, pp. 9278- 9293 ,(2007) , 10.1523/JNEUROSCI.2826-07.2007
Alexander Y. Andreyev, Brenda Fahy, Gary Fiskum, Cytochrome c release from brain mitochondria is independent of the mitochondrial permeability transition FEBS Letters. ,vol. 439, pp. 373- 376 ,(1998) , 10.1016/S0014-5793(98)01394-5
Marja Jäättelä, Programmed cell death: many ways for cells to die decently Annals of Medicine. ,vol. 34, pp. 480- 488 ,(2002) , 10.1080/078538902321012423
Pierluigi Nicotera, Marcel Leist, Luigi Manzo, Neuronal cell death: a demise with different shapes Trends in Pharmacological Sciences. ,vol. 20, pp. 46- 51 ,(1999) , 10.1016/S0165-6147(99)01304-8
Hans K. Lorenzo, Santos A. Susin, Therapeutic potential of AIF-mediated caspase-independent programmed cell death Drug Resistance Updates. ,vol. 10, pp. 235- 255 ,(2007) , 10.1016/J.DRUP.2007.11.001
S Alford, B G Frenguelli, J G Schofield, G L Collingridge, Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors. The Journal of Physiology. ,vol. 469, pp. 693- 716 ,(1993) , 10.1113/JPHYSIOL.1993.SP019838