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

Galluzzi, L; Bravo-San Pedro, JM; Vitale, I; Aaronson, SA; Abrams, JM; Adam, D; Alnemri, ES; ... Kroemer, G; + view all (2015) Essential versus accessory aspects of cell death: recommendations of the NCCD 2015. Cell Death and Differentiation , 22 (1) pp. 58-73. 10.1038/cdd.2014.137. Green open access

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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.

Type: Article
Title: Essential versus accessory aspects of cell death: recommendations of the NCCD 2015
Open access status: An open access version is available from UCL Discovery
DOI: 10.1038/cdd.2014.137
Publisher version: http://dx.doi.org/10.1038/cdd.2014.137
Language: English
Additional information: Copyright © 2017 ADMC Associazione Differenziamento e Morte Cellulare This work is licensed under a Creative Commons Attribution 3.0 Unported License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/.
Keywords: Mitochondrial Permeability Transition, Tumor-necrosis-factor, Apoptosis-inducing Factor, Mixed Lineage Kinase, Cytochrome-c Release, Ischemia-reperfusion Injury, Domain-like Protein, Q-vd-oph, Outer-membrane Permeabilization, Caspase Inhibition Switches
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences > Cell and Developmental Biology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Cancer Bio
URI: https://discovery.ucl.ac.uk/id/eprint/1450355
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