Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012
Open accessAbstract
In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.
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Claim (b) is stronger than claim (a) and needs proof that inhibiting autophagy prevents cell death.
“Clearly claim (b) is stronger than claim (a), and needs to be justified by proof that inhibiting autophagy, through either genetic or chemical means, prevents cell death.669”
From Guidelines for the use and interpretation of assays for monitoring autophagy (2012) · cites this paper as [669]
The apoptosis induced by the combination of etoposide and Nutlin 3a is caspase-independent.
“arguing for caspase-independent apoptosis.43”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [43]
PCD and necrosis mechanisms can sometimes overlap, and necrosis is a more regulated process than was previously assumed.
“However, more recently it has become clear that the PCD and necrosis mechanisms can sometimes overlap, and that necrosis is a more regulated process than was previously assumed(Galluzzi et al., 2012).”
From Programmed cell death in aging (2015) · cites this paper as Galluzzi et al., 2012
Macroautophagy is typically a protective and anti-apoptotic mechanism, and therefore autophagic cell death may involve hyper-activation of a normally beneficial process.
“Notably, macroautophagy is typically a protective and anti-apoptotic mechanism, and therefore autophagic cell death may involve hyper-activation of a normally beneficial process.”
From Programmed cell death in aging (2015) · cites this paper as Galluzzi et al., 2012
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“…deficiency can be rescued by concurrent deletion of RIPK3 (Kaiser et al., 2011; Oberst et al., 2011), a kinase that promotes a form of programmed necrotic cell death (sometimes called “necroptosis” (Galluzzi et al., 2012)), indicating a more specific and limited role for caspase-8 in development.”
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Self-citation
- Authors
- Galluzzi, L., Vitale, I., Abrams, J. M., Alnemri, E. S., Baehrecke, E. H., Blagosklonny, M. V., Dawson, T. M., Dawson, V. L., El-Deiry, W. S., Fulda, S., Gottlieb, E., Green, D. R., Hengartner, M. O., Kepp, O., Knight, R. A., Kumar, S., Lipton, S. A., Lu, X., Madeo, F., Malorni, W., Mehlen, P., Nuñez, G., Peter, M. E., Piacentini, M., Rubinsztein, D. C., Shi, Y., Simon, H.-U., Vandenabeele, P., White, E., Yuan, J., Zhivotovsky, B., Melino, G., & Kroemer, G.
- Affiliations
- Inserm (FR)
- Université Paris-Sud (FR)
- The University of Texas Southwestern Medical Center (US)
- Thomas Jefferson University (US)
- University of Massachusetts Chan Medical School (US)
- Roswell Park Comprehensive Cancer Center (US)
- Johns Hopkins University (US)
- Goethe University Frankfurt (DE)
- Cancer Research UK Scotland Institute (GB)
- St. Jude Children's Research Hospital (US)
- University of Zurich (CH)
- University College London (GB)
- South Australia Pathology (AU)
- Scripps Research Institute (US)
- University of Graz (AT)
- Istituto Superiore di Sanità (IT)
- Centre National de la Recherche Scientifique (FR)
- Northwestern University (US)
- University of Rome Tor Vergata (IT)
- University of Cambridge (GB)
- Shanghai Institutes for Biological Sciences (CN)
- University of Bern (CH)
- Vlaams Instituut voor Biotechnologie (BE)
- Rutgers Cancer Institute (US)
- Harvard University (US)
- Karolinska Institutet (SE)
- Corresponding author
- Kroemer, G
- ORCID
- Venue
- Cell Death & Differentiation
- Published
- 2011-07-15
- Volume
- 19
- Issue
- 1
- Pages
- 107-120
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- PMC
- PMC3252826
- OpenAlex
- W2030864103
- Cited by
- 2,421
- References
- 186
- Citations by year
- 2026: 38 · 2025: 64 · 2024: 87 · 2023: 116 · 2022: 123 · 2021: 138 · 2020: 111 · 2019: 148 · 2018: 174 · 2017: 185 · 2016: 258 · 2015: 275 · 2014: 262 · 2013: 263 · 2012: 153
- FWCI
- 20.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Death and Differentiation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Bern Open Repository and Information System (University of Bern) (submittedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- Wellcome Trust
- National Institute of General Medical Sciences (R01GM072124, R01GM079431)
- National Institute of Neurological Disorders and Stroke (P50NS038377, R01NS067525)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Social Sciences › Anthropology › Death, Funerary Practices, and Mourning
- Keywords
- cell death, apoptosis, regulated necrosis, autophagic cell death, mitotic catastrophe, caspase-dependent apoptosis, caspase-independent apoptosis, extrinsic apoptotic pathway
- MeSH terms
- Animals, Autophagy, Cells, Humans, Mitosis, Necrosis, Terminology as Topic, Apoptosis, Caspases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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