Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

被引：784

作者：

Galluzzi, L. ^{[1
,2
,3
]}

Bravo-San Pedro, J. M. ^{[1
,2
,4
]}

Vitale, I. ^{[5
]}

Aaronson, S. A. ^{[6
]}

Abrams, J. M. ^{[7
]}

Adam, D. ^{[8
]}

Alnemri, E. S. ^{[9
]}

Altucci, L. ^{[10
]}

Andrews, D. ^{[11
]}

Annicchiarico-Petruzzelli, M. ^{[12
]}

Baehrecke, E. H. ^{[13
]}

Bazan, N. G. ^{[14
]}

Bertrand, M. J. ^{[15
,16
]}

Bianchi, K. ^{[17
,18
]}

Blagosklonny, M. V. ^{[19
]}

Blomgren, K. ^{[20
]}

Borner, C. ^{[21
,22
]}

Bredesen, D. E. ^{[23
,24
]}

Brenner, C. ^{[25
,26
,27
]}

Campanella, M. ^{[28
,29
]}

Candi, E. ^{[30
]}

Cecconi, F. ^{[31
,32
,33
]}

Chan, F. K. ^{[34
]}

Chandel, N. S. ^{[35
]}

Cheng, E. H. ^{[36
,37
]}

Chipuk, J. E. ^{[6
]}

Cidlowski, J. A. ^{[38
]}

Ciechanover, A. ^{[39
]}

Dawson, T. M. ^{[40
,41
]}

Dawson, V. L. ^{[40
,41
]}

De laurenzi, V. ^{[42
]}

De Maria, R. ^{[5
]}

Debatin, K-M ^{[43
]}

Di Daniele, N. ^{[44
]}

Dixit, V. M. ^{[45
]}

Dynlacht, B. D. ^{[46
,47
]}

El-Deiry, W. S. ^{[48
]}

Fimia, G. M. ^{[49
,50
]}

Flavell, R. A. ^{[51
]}

Fulda, S. ^{[52
]}

Garrido, C. ^{[53
,54
]}

Gougeon, M-L ^{[55
]}

Green, D. R. ^{[56
]}

Gronemeyer, H. ^{[57
]}

Hajnoczky, G. ^{[58
]}

Hardwick, J. M. ^{[59
]}

Hengartner, M. O. ^{[60
]}

Ichijo, H. ^{[61
]}

Joseph, B. ^{[62
]}

Jost, P. J. ^{[63
]}

机构：

[1] Gustave Roussy Canc Ctr, Villejuif, France

[2] Ctr Rech Cordeliers, Equipe Labellisee Ligue Natl Contre Canc 11, F-75006 Paris, France

[3] Univ Paris 05, Sorbonne Paris Cite, Paris, France

[4] Gustave Roussy, INSERM, U1138, Paris, France

[5] Regina Elena Inst Canc Res, Rome, Italy

[6] Icahn Sch Med Mt Sinai, Tisch Canc Inst, Dept Oncol Sci, New York, NY 10029 USA

[7] UT Southwestrn Med Ctr, Dept Cell Biol, Dallas, TX USA

[8] Univ Kiel, Inst Immunol, Kiel, Germany

[9] Thomas Jefferson Univ, Dept Biochem & Mol Biol, Philadelphia, PA 19107 USA

[10] Seconda Univ Napoli, Dipartimento Biochim Biofis & Patol Gen, Naples, Italy

[11] Univ Toronto, Dept Biochem & Med Biophys, Toronto, ON, Canada

[12] IRCCS, IDI, Biochem Lab, Rome, Italy

[13] Univ Massachusetts, Sch Med, Dept Canc Biol, Worcester, MA USA

[14] Sch Med, Neurosci Ctr Excellence, New Orleans, LA USA

[15] VIB, Inflammat Res Ctr, Ghent, Belgium

[16] Univ Ghent, Dept Biomed Mol Biol, B-9000 Ghent, Belgium

[17] Canc Res UK Ctr Excellence, Barts Canc Inst, London, England

[18] Queen Mary Univ London, John Vane Sci Ctr, London, England

[19] Roswell Pk Canc Inst, Dept Cell Stress Biol, Buffalo, NY 14263 USA

[20] Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden

[21] Univ Freiburg, Inst Mol Med, D-79106 Freiburg, Germany

[22] Univ Freiburg, Spemann Grad Sch Biol & Med, D-79106 Freiburg, Germany

[23] Buck Inst Res Aging, Novato, CA USA

[24] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

[25] INSERM, UMRS769, Chatenay Malabry, France

[26] LabEx LERMIT, Chatenay Malabry, France

[27] Univ Paris 11, Orsay, France

[28] UCL, Dept Comparat Biomed Sci, London, England

[29] UCL, Consortium Mitochondrial Res, London, England

[30] Univ Roma Tor Vergata, Dept Expt Med & Surg, Rome, Italy

[31] IRCCS Fdn Santa Lucia, Lab Mol Neuroembryol, Rome, Italy

[32] Univ Roma Tor Vergata, Dept Biol, I-00173 Rome, Italy

[33] Danish Canc Soc Res Ctr, Unit Cell Stress & Survival, Copenhagen, Denmark

[34] Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01605 USA

[35] Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA

[36] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10021 USA

[37] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA

[38] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC USA

[39] Technion Israel Inst Technol, Rappaport Fac Med & Res Inst, Tumor & Vasc Biol Res Ctr, Haifa, Israel

[40] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Solomon H Snyder Dept Neurosci,Dept Neurol Pharma, Baltimore, MD USA

[41] Adrienne Helis Malvin Med Res Fdn, New Orleans, LA USA

[42] Gabriele Annunzio Univ, Dept Expt & Clin Sci, Chieti, Italy

[43] Ulm Univ Med Ctr, Dept Pediat & Adolescent Med, Ulm, Germany

[44] Univ Roma Tor Vergata, Dept Syst Med, Rome, Italy

[45] Genentech Inc, Dept Physiol Chem, South San Francisco, CA USA

[46] NYU, Sch Med, Smilow Res Ctr, Dept Pathol, New York, NY USA

[47] NYU, Sch Med, Smilow Res Ctr, Inst Canc, New York, NY USA

[48] Penn State Coll Med, Penn State Hershey Canc Inst, Dept Med Hematol Oncol, Lab Translat Oncol & Expt Canc Therapeut, Hershey, PA USA

[49] Univ Salento, Dept Biol & Environm Sci & Technol DiSTeBA, Lecce, Italy

[50] IRCCS, Natl Inst Infect Dis Lazzaro Spallanzani, Dept Epidemiol & Preclin Res, Rome, Italy

来源：

CELL DEATH AND DIFFERENTIATION | 2015年 / 22卷 / 01期

基金：

英国生物技术与生命科学研究理事会;

关键词：

MITOCHONDRIAL PERMEABILITY TRANSITION; TUMOR-NECROSIS-FACTOR; MIXED LINEAGE KINASE; APOPTOSIS-INDUCING FACTOR; CYTOCHROME-C RELEASE; DOMAIN-LIKE PROTEIN; Q-VD-OPH; CASPASE INHIBITION SWITCHES; PROGRAMMED NECROSIS; CYCLOPHILIN-D;

D O I：

10.1038/cdd.2014.137

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：

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

引用

页码：58 / 73

页数：16

共 336 条

[1] An uncoupling channel within the c-subunit ring of the F1FO ATP synthase is the mitochondrial permeability transition pore [J].