The DOI matches its Crossref record; 190 of the 190 references it cites were found in a registry or an index.
Programmed Necrosis in the Cross Talk of Cell Death and Inflammation
Open accessAbstract
Cell proliferation and cell death are integral elements in maintaining homeostatic balance in metazoans. Disease pathologies ensue when these processes are disturbed. A plethora of evidence indicates that malfunction of cell death can lead to inflammation, autoimmunity, or immunodeficiency. Programmed necrosis or necroptosis is a form of nonapoptotic cell death driven by the receptor interacting protein kinase 3 (RIPK3) and its substrate, mixed lineage kinase domain-like (MLKL). RIPK3 partners with its upstream adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cell injury. Necroptosis promotes inflammation through leakage of cellular contents from damaged plasma membranes. Intriguingly, many of the signal adaptors of necroptosis have dual functions in innate immune signaling. This unique signature illustrates the cooperative nature of necroptosis and innate inflammatory signaling pathways in managing cell and organismal stresses from pathogen infection and sterile tissue injury.
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Citations
Cites
NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice
Heneka, M. T., Kummer, M. P., Stutz, A., Delekate, A., Schwartz, S., Vieira-Saecker, A., Griep, A., Axt, D., Remus, A., Tzeng, T.-C., et al. (2013) · Nature · doi:10.1038/nature11729 · Cited by 2,898
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Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase
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The NALP3 inflammasome is involved in the innate immune response to amyloid-β
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Self-citationReceptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α
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“As such, Ripk3−/− and Mlkl−/− mice are partially protected from cerulein-induced acute pancreatitis (153, 168).”
BackgroundIdentification of RIP1 kinase as a specific cellular target of necrostatins
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RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis
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Cited by
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
Self-citationChen, X., He, W.-T., Hu, L., Li, J., Fang, Y., Wang, X., Xu, X., Wang, Z., Huang, K., & Han, J. (2016) · Cell Research · doi:10.1038/cr.2016.100 · Cited by 831
Zhang, Y., Su, S. S., Zhao, S., Yang, Z., Zhong, C.-Q., Chen, X., Cai, Q., Yang, Z.-H., Huang, D., Wu, R., et al. (2017) · Nature Communications · doi:10.1038/ncomms14329 · Cited by 599
Initiation and execution mechanisms of necroptosis: an overview
Grootjans, S., Vanden Berghe, T., & Vandenabeele, P. (2017) · Cell Death & Differentiation · doi:10.1038/cdd.2017.65 · Cited by 566
Jiao, Y., Zhang, T., Zhang, C., Ji, H., Tong, X., Xia, R., Wang, W., Ma, Z., & Shi, X. (2021) · Critical Care · doi:10.1186/s13054-021-03775-3 · Cited by 558
Metadata
- Authors
- Chan, F. K.-M., Luz, N. F., & Moriwaki, K.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2015-03-21
- Volume
- 33
- Issue
- 1
- Pages
- 79-106
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2159679709
- Cited by
- 351
- References
- 190
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- green
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- Chan, F. K.-M., Luz, N. F., & Moriwaki, K. (2015). Programmed Necrosis in the Cross Talk of Cell Death and Inflammation. Annual Review of Immunology. https://doi.org/10.1146/annurev-immunol-032414-112248
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