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

By L. Galluzzi, J. M. Bravo-San Pedro, Ilio Vitale, S. Aaronson, J. Abrams, D. Adam, E. Alnemri, L. Altucci, David W. Andrews, M. Annicchiarico-Petruzzelli and 98 more. Cell Death and Differentiation, 2014

970 citations recorded by the source corpus.

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.

Subfields: Epidemiology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b1eede3cab7e141dbb7db4524254170491c4b1ca

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Citations in the corpus

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. (2017, neutral): “…pharmacologically and genetically, and is therefore under the control of specific biological mechanisms; moreover, the NCCD notes that programmed cell death is a subset of regulated cell death that is predestined to occur in normal physiological contexts such as development (Galluzzi et al., 2015).”
Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “21,148 ; 2) The vulnerability of immune cells to ferroptosis compromises their anti-tumor function or enhances their pro-tumor effect, leading to tumor growth.”
Autophagy in malignant transformation and cancer progression (2015, positive): “This said, regulated instances of cell death that causally depend on the autophagic machinery have been described (Denton et al , 2009; Denton et al , 2012b; Liu et al , 2013b; Galluzzi et al , 2015).”
The molecular machinery of regulated cell death (2019, neutral): “Currently, cell death can be fundamentally divided into accidental cell death (ACD) and RCD, based on functional aspects.(23) ACD can be triggered by unexpected attack and injury that overwhelms any possible control mechanisms.”
FerrDb: a manually curated resource for regulators and markers of ferroptosis and ferroptosis-disease associations (2020, background): “To view a gene’s regulation pathway in ferroptosis, a ‘View’ button in the ‘Pathway’ column is provided, as illustrated in the inset (2) in Figure 3.”