The DOI matches its Crossref record; 126 of the 130 references it cites were found in a registry or an index.
Die another way – non-apoptotic mechanisms of cell death
Open accessAbstract
Regulated, programmed cell death is crucial for all multicellular organisms. Cell death is essential in many processes, including tissue sculpting during embryogenesis, development of the immune system and destruction of damaged cells. The best-studied form of programmed cell death is apoptosis, a process that requires activation of caspase proteases. Recently it has been appreciated that various non-apoptotic forms of cell death also exist, such as necroptosis and pyroptosis. These non-apoptotic cell death modalities can be either triggered independently of apoptosis or are engaged should apoptosis fail to execute. In this Commentary, we discuss several regulated non-apoptotic forms of cell death including necroptosis, autophagic cell death, pyroptosis and caspase-independent cell death. We outline what we know about their mechanism, potential roles in vivo and define outstanding questions. Finally, we review data arguing that the means by which a cell dies actually matters, focusing our discussion on inflammatory aspects of cell death.
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“In contrast to the highly pro-inflammatory necrotic types of cell death, such as necroptosis and pyroptosis, apoptosis and autophagy do not tend to trigger an inflammatory response166.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [166]
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Cites
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Wei, M. C., Zong, W.-X., Cheng, E. H.-Y., Lindsten, T., Panoutsakopoulou, V., Ross, A. J., Roth, K. A., MacGregor, G. R., Thompson, C. B., & Korsmeyer, S. J. (2001) · Science · doi:10.1126/science.1059108 · Cited by 3,988
Bcl-2 Antiapoptotic Proteins Inhibit Beclin 1-Dependent Autophagy
Pattingre, S., Tassa, A., Qu, X., Garuti, R., Liang, X. H., Mizushima, N., Packer, M., Schneider, M. D., & Levine, B. (2005) · Cell · doi:10.1016/j.cell.2005.07.002 · Cited by 3,536
Pyroptosis: host cell death and inflammation
Bergsbaken, T., Fink, S. L., & Cookson, B. T. (2009) · Nature Reviews Microbiology · doi:10.1038/nrmicro2070 · Cited by 3,288
Calreticulin exposure dictates the immunogenicity of cancer cell death
Obeid, M., Tesniere, A., Ghiringhelli, F., Fimia, G. M., Apetoh, L., Perfettini, J.-L., Castedo, M., Mignot, G., Panaretakis, T., Casares, N., et al. (2007) · Nature Medicine · doi:10.1038/nm1523 · Cited by 3,216
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
Degterev, A., Huang, Z., Boyce, M., Li, Y., Jagtap, P., Mizushima, N., Cuny, G. D., Mitchison, T. J., Moskowitz, M. A., & Yuan, J. (2005) · Nature Chemical Biology · doi:10.1038/nchembio711 · Cited by 3,068
Apoptosis: controlled demolition at the cellular level
Taylor, R. C., Cullen, S. P., & Martin, S. J. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2312 · Cited by 2,708
Caspase Functions in Cell Death and DiseasePreprint
McIlwain, D. R., Berger, T., & Mak, T. W. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a008656 · Cited by 2,702
Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase
Sun, L., Wang, H., Wang, Z., He, S., Chen, S., Liao, D., Wang, L., Yan, J., Liu, W., Lei, X., et al. (2012) · Cell · doi:10.1016/j.cell.2011.11.031 · Cited by 2,698
Autophagy in Human Health and Disease
Choi, A. M. K., Ryter, S. W., & Levine, B. (2013) · New England Journal of Medicine · doi:10.1056/nejmra1205406 · Cited by 2,583
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“Taken together with the notion that the absence of either Ripk3, Casp8 or Fadd fails to rescue Ripk1 / mice from neonatal lethality,(180,185) these results pointed to the existence of a switch mechanism that regulates cell fate upon TNFR1 ligation.(204,205) Intriguingly, such switch may not operate in all cell types,…”
BackgroundSelf-citationApoptotic Caspases Prevent the Induction of Type I Interferons by Mitochondrial DNA
Rongvaux, A., Jackson, R., Harman, C. C. D., Li, T., West, A. P., de Zoete, M. R., Wu, Y., Yordy, B., Lakhani, S. A., Kuan, C.-Y., et al. (2014) · Cell · doi:10.1016/j.cell.2014.11.037 · Cited by 847
“2008; Callus and Vaux, 2007; Tait et al., 2014).”
BackgroundInfluentialMitochondrial apoptosis: killing cancer using the enemy within
Lopez, J., & Tait, S. W. G. (2015) · British Journal of Cancer · doi:10.1038/bjc.2015.85 · Cited by 817
“Importantly, MOMP often leads to cell death irrespective of caspase activity (Tait et al, 2014).”
BackgroundSelf-citation
Metadata
- Authors
- Tait, S. W. G., Ichim, G., & Green, D. R.
- Affiliations
- Cancer Research UK Scotland Institute (GB)
- St. Jude Children's Research Hospital (US)
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2014-05-15
- Volume
- 127
- Issue
- 10
- Pages
- 2135-2144
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- PMC
- PMC4021468
- OpenAlex
- W2021358525
- Cited by
- 366
- References
- 130
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 21 · 2023: 14 · 2022: 26 · 2021: 34 · 2020: 41 · 2019: 48 · 2018: 40 · 2017: 43 · 2016: 35 · 2015: 30 · 2014: 5
- FWCI
- 3.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cell Science (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Biotechnology and Biological Sciences Research Council (BB/K008374/1)
- National Institute of General Medical Sciences (R01GM096208)
- National Institute of Allergy and Infectious Diseases (R01AI044828)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- non-apoptotic cell death, programmed cell death, necroptosis, pyroptosis, autophagic cell death, caspase-independent cell death, apoptosis, inflammation, immune system development
- MeSH terms
- Animals, Autophagy, Humans, Cell Death, Apoptosis
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