Necroptosis: The Release of Damage-Associated Molecular Patterns and Its Physiological Relevance
Open accessAbstract
Regulated necrosis, termed necroptosis, is negatively regulated by caspase-8 and is dependent on the kinase activity of RIPK1 and RIPK3. Necroptosis leads to rapid plasma membrane permeabilization and to the release of cell contents and exposure of damage-associated molecular patterns (DAMPs). We are only beginning to identify the necroptotic DAMPs, their modifications, and their potential role in the regulation of inflammation. In this review, we discuss the physiological relevance of necroptosis and its role in the modulation of inflammation. For example, during viral infection, RIPK3-mediated necroptosis acts as a backup mechanism to clear pathogens. Necroptosis is also involved in apparently immunologically silent maintenance of T cell homeostasis. In contrast, the induction of necroptosis in skin, intestine, systemic inflammatory response syndrome, and ischemia reperfusion injury provoke a strong inflammatory response, which might be triggered by emission of DAMPs from necroptotic cells, showing the detrimental side of necroptosis.
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Necroptosis triggers inflammation through the massive release of DAMPs from the disintegrating cell.
“However, necroptosis triggers inflammation through the massive release of DAMPs from the disintegrating cell.237”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [237]
The Introduction says inflammation in necroptosis-associated disease can be attributed at least partly to DAMP release, and the DAMP-signatures section describes spillage of necroptotic cell contents. But “triggers inflammation through the massive release” states the mechanism more definitively than the paper does: The Silent and Proinflammatory Faces of Necroptosis reports examples that did not elicit inflammatory responses, while the Concluding Remarks say DAMPs’ precise role remains unknown. The supplied passages do not establish that the release is massive. (LLM, conf=0.88)
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References 129 · Cited by 1,411
Research works printed but not linked: 1
- Lu, J.V., Weist, B.M., van Raam, B.J., Marro, B.S., Nguyen, L.V., Srinivas, P., Bell, B.D., Luhrs, K.A., Lane, T.E., Salvesen, G.S., and Walsh, C.M. (2011b). Complementary roles of Fas-associated death domain (FADD) and receptor interacting protein kinase-3 (RIPK3) in T-cell homeostasis and antiviral immunity. Proc. Natl. Acad. Sci. USA 108, 15312-15317.
- Authors
- Kaczmarek, A., Vandenabeele, P., & Krysko, D. V.
- Affiliations
- Ghent University (BE)
- Corresponding author
- Vandenabeele, Peter
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 38
- Issue
- 2
- Pages
- 209-223
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1966977448
- Cited by
- 1,411
- References
- 129
- Citations by year
- 2026: 81 · 2025: 96 · 2024: 115 · 2023: 126 · 2022: 132 · 2021: 119 · 2020: 109 · 2019: 92 · 2018: 112 · 2017: 76 · 2016: 97 · 2015: 97 · 2014: 109 · 2013: 48
- FWCI
- 11.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Funders
- Fonds Wetenschappelijk Onderzoek
- Servier
- Vlaamse regering
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- necroptosis, regulated necrosis, damage-associated molecular patterns, caspase-8, RIPK1, RIPK3, plasma membrane permeabilization, inflammation, viral infection, T cell homeostasis, systemic inflammatory response syndrome, ischemia-reperfusion injury, intestinal inflammation, skin inflammation
- MeSH terms
- Animals, Bacteria, Bacterial Infections, Humans, Inflammation, Necrosis, T-Lymphocytes, Virus Diseases, Viruses, Reperfusion Injury, Apoptosis, Receptors, Pattern Recognition, Caspase 8, Receptor-Interacting Protein Serine-Threonine Kinases
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