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

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Abstract
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.
Keywords
TUMOR-NECROSIS-FACTOR, MITOCHONDRIAL PERMEABILITY TRANSITION, APOPTOSIS-INDUCING FACTOR, MIXED LINEAGE KINASE, CYTOCHROME-C RELEASE, ISCHEMIA-REPERFUSION INJURY, DOMAIN-LIKE PROTEIN, Q-VD-OPH, OUTER-MEMBRANE PERMEABILIZATION, CASPASE INHIBITION SWITCHES

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Chicago
Galluzzi, L, JM Bravo-San Pedro, I Vitale, SA Aaronson, JM Abrams, D Adam, ES Alnemri, et al. 2015. “Essential Versus Accessory Aspects of Cell Death: Recommendations of the NCCD 2015.” Cell Death and Differentiation 22 (1): 58–73.
APA
Galluzzi, L, Bravo-San Pedro, J., Vitale, I., Aaronson, S., Abrams, J., Adam, D., Alnemri, E., et al. (2015). Essential versus accessory aspects of cell death: recommendations of the NCCD 2015. CELL DEATH AND DIFFERENTIATION, 22(1), 58–73.
Vancouver
1.
Galluzzi L, Bravo-San Pedro J, Vitale I, Aaronson S, Abrams J, Adam D, et al. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015. CELL DEATH AND DIFFERENTIATION. 2015;22(1):58–73.
MLA
Galluzzi, L, JM Bravo-San Pedro, I Vitale, et al. “Essential Versus Accessory Aspects of Cell Death: Recommendations of the NCCD 2015.” CELL DEATH AND DIFFERENTIATION 22.1 (2015): 58–73. Print.
@article{5818701,
  abstract     = {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.},
  author       = {Galluzzi, L and Bravo-San Pedro, JM and Vitale, I and Aaronson, SA and Abrams, JM and Adam, D and Alnemri, ES and Altucci, L and Andrews, D and Annicchiarico-Petruzzelli, M and Baehrecke, EH and Bazan, NG and Bertrand, Mathieu and Bianchi, K and Blagosklonny, MV and Blomgren, K and Borner, C and Bredesen, DE and Brenner, C and Campanella, M and Candi, E and Cecconi, F and Chan, FK and Chandel, NS and Cheng, EH and Chipuk, JE and Cidlowski, JA and Ciechanover, A and Dawson, TM and Dawson, VL and De Laurenzi, V and De Maria, R and Debatin, K-M and Di Daniele, N and Dixit, VM and Dynlacht, BD and El-Deiry, WS and Fimia, GM and Flavell, RA and Fulda, S and Garrido, C and Gougeon, M-L and Green, DR and Gronemeyer, H and Hajnoczky, G and Hardwick, JM and Hengartner, MO and Ichijo, H and Joseph, B and Jost, PJ and Kaufmann, T and Kepp, O and Klionsky, DJ and Knight, RA and Kumar, S and Lemasters, JJ and Levine, B and Linkermann, A and Lipton, SA and Lockshin, RA and L{\'o}pez-Ot{\'i}n, C. and Lugli, E and Madeo, F and Malorni, W and Marine, J-C and Martin, SJ and Martinou, J-C and Medema, JP and Meier, P and Melino, S and Mizushima, N and Moll, U and Mu{\~n}oz-Pinedo, C and Nu{\~n}ez, G and Oberst, A and Panaretakis, T and Penninger, JM and Peter, ME and Piacentini, M and Pinton, P and Prehn, JH and Puthalakath, H and Rabinovich, GA and Ravichandran, KS and Rizzuto, R and Rodrigues, CM and Rubinsztein, DC and Rudel, T and Shi, Y and Simon, H-U and Stockwell, BR and Szabadkai, G and Tait, SW and Tang, HL and Tavernarakis, N and Tsujimoto, Y and Vanden Berghe, Tom and Vandenabeele, Peter and Villunger, A and Wagner, EF and Walczak, H and White, E and Wood, WG and Yuan, J and Zakeri, Z and Zhivotovsky, B and Melino, G and Kroemer, G},
  issn         = {1350-9047},
  journal      = {CELL DEATH AND DIFFERENTIATION},
  keyword      = {TUMOR-NECROSIS-FACTOR,MITOCHONDRIAL PERMEABILITY TRANSITION,APOPTOSIS-INDUCING FACTOR,MIXED LINEAGE KINASE,CYTOCHROME-C RELEASE,ISCHEMIA-REPERFUSION INJURY,DOMAIN-LIKE PROTEIN,Q-VD-OPH,OUTER-MEMBRANE PERMEABILIZATION,CASPASE INHIBITION SWITCHES},
  language     = {eng},
  number       = {1},
  pages        = {58--73},
  title        = {Essential versus accessory aspects of cell death: recommendations of the NCCD 2015},
  url          = {http://dx.doi.org/10.1038/cdd.2014.137},
  volume       = {22},
  year         = {2015},
}

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