The DOI matches its Crossref record; 150 of the 150 references it cites were found in a registry or an index.
Crosstalk between apoptosis.; necrosis and autophagy
Open accessAbstract
Apoptosis and necrosis are the two major modes of cell death, the molecular mechanisms of which have been extensively studied. Although initially thought to constitute mutually exclusive cellular states, recent findings reveal cellular contexts that require a balanced interplay between these two modes of cellular demise. Several death initiator and effector molecules, signaling pathways and subcellular sites have been identified as key mediators in both processes, either by constituting common modules or alternatively by functioning as a switch allowing cells to decide which route to take, depending on the specific situation. Importantly, autophagy, which is a predominantly cytoprotective process, has been linked to both types of cell death, serving either a pro-survival or pro-death function. Here we review the recent literature that highlights the intricate interplay between apoptosis, necrosis and autophagy, focusing on the relevance and impact of this crosstalk in normal development and in pathology. This article is part of a Special Section entitled: Cell Death Pathways.
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“While autophagy is implicated in several paradigms of life extension and is generally considered an antiaging mechanism, autophagy is also a well-defined mechanism of cell death, autophagy-dependent cell death, ADCD [153,154,155].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [153]
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1 retracted
The NAD-dependent deacetylase SIRT2 is required for programmed necrosis
Narayan, N., Lee, I. H., Borenstein, R., Sun, J., Wong, R. P., Tong, G., Fergusson, M. M., Liu, J., Rovira, I. I., Cheng, H.-L., et al. (2012) · Nature · doi:10.1038/nature11700 · Cited by 136 · cited 2×
“Recent fi ndings indicate that SIRT2 is also involved in the regulation of necroptosis [130].”
BackgroundRetractedApoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics
Kerr, J. F. R., Wyllie, A. H., & Currie, A. R. (1972) · British Journal of Cancer · doi:10.1038/bjc.1972.33 · Cited by 15,673
p53, the cellular gatekeeper for growth and division
Levine, A. J. (1997) · Cell · doi:10.1016/s0092-8674(00)81871-1 · Cited by 7,693
AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1
Kim, J., Kundu, M., Viollet, B., & Guan, K.-L. (2011) · Nature Cell Biology · doi:10.1038/ncb2152 · Cited by 7,227 · cited 1×
“3; [135,136]), or through activation of theULK1complex[137,138].”
Cell Death: The Significance of Apoptosis
Wyllie, A. H., Kerr, J. F. R., & Currie, A. R. (1980) · International review of cytology · doi:10.1016/s0074-7696(08)62312-8 · Cited by 7,151 · cited 1×
“Mechanistically, necrosis is typically not associated with activation of caspases, and it is thought that it mediates cell demise in response to damage, or in pathology [10,11], but not during normal development.”
BackgroundAutophagy in the Pathogenesis of Disease
Levine, B., & Kroemer, G. (2008) · Cell · doi:10.1016/j.cell.2007.12.018 · Cited by 7,069 · cited 1×
“Completion of the autophagosome is followed by fusion with a lysosome to form an autolysosome, where the captured material is degraded by specific acidic hydrolases [12].”
BackgroundAutophagy fights disease through cellular self-digestion
Mizushima, N., Levine, B., Cuervo, A. M., & Klionsky, D. J. (2008) · Nature · doi:10.1038/nature06639 · Cited by 6,452 · cited 1×
“Although it is primarily considered to have a cytoprotective function, autophagy can also promote cell death during normal development (reviewed in [13]), as well as, in disease (reviewed in [14]).”
BackgroundTOR signaling in growth and metabolism
Wullschleger, S., Loewith, R., & Hall, M. N. (2006) · Cell · doi:10.1016/j.cell.2006.01.016 · Cited by 5,787 · cited 1×
“Low insulin – IGF1 signaling, nutrient or energy limitation and stress converge to downregulate the activity of TOR [83].”
BackgroundCellular survival: a play in three Akts
Datta, S. R., Brunet, A., & Greenberg, M. E. (1999) · Genes & Development · doi:10.1101/gad.13.22.2905 · Cited by 4,216 · cited 1×
“AKT ability to prevent apoptosis in some cells is established through phosphorylation and inhibition of pro-apoptotic mediators such as Bad and caspase-9 [44].”
BackgroundTSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
Inoki, K., Zhu, T., & Guan, K.-L. (2003) · Cell · doi:10.1016/s0092-8674(03)00929-2 · Cited by 3,914 · cited 1×
“3; [135,136]), or through activation of theULK1complex[137,138].”
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Schmidt, S., Schubert, R., Tramsen, L., & Lehrnbecher, T. (2019) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01993-18 · Cited by 5
“However, comparable to that with other cellular therapies, a sufficient number of vital and functionally active effector cells are a prerequisite for clinical efficacy (9).”
Background
Metadata
- Authors
- Nikoletopoulou, V., Markaki, M., Palikaras, K., & Tavernarakis, N.
- Affiliations
- Foundation for Research and Technology Hellas (GR)
- Corresponding author
- Tavernarakis, Nektarios
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 1833
- Issue
- 12
- Pages
- 3448-3459
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2059738518
- Cited by
- 1,366
- References
- 150
- Citations by year
- 2026: 43 · 2025: 58 · 2024: 80 · 2023: 91 · 2022: 113 · 2021: 147 · 2020: 133 · 2019: 146 · 2018: 136 · 2017: 141 · 2016: 122 · 2015: 107 · 2014: 43 · 2013: 5
- FWCI
- 8.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- European Research Council
- Ministry of National Education and Religious Affairs
- European Molecular Biology Organization
- Seventh Framework Programme
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Social Sciences › Anthropology › Death, Funerary Practices, and Mourning
- Keywords
- apoptosis, necrosis, autophagy, cell death crosstalk, cell death pathways, cell fate determination, development (biology), disease pathology
- MeSH terms
- Autophagy, Humans, Models, Biological, Necrosis, Signal Transduction, Apoptosis
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