Vesicular stomatitis virus, a single-stranded RNA virus, triggers activation of the serine-threonine kinases RIP1 and RIP3, which damages mitochondria by activating the GTPase DRP1. This results in excessive production of reactive oxygen species and subsequent activation of the NLRP3 inflammasome.
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Activated Drp1 regulates p62-mediated autophagic flux and aggravates inflammation in cerebral ischemia-reperfusion via the ROS-RIP1/RIP3-exosome axis
Military Medical Research Open Access 27 May 2022
-
A surfactant polymer wound dressing protects human keratinocytes from inducible necroptosis
Scientific Reports Open Access 23 February 2021
-
The kinase receptor-interacting protein 1 is required for inflammasome activation induced by endoplasmic reticulum stress
Cell Death & Disease Open Access 29 May 2018
Access options
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Change history
10 April 2015
In the version of this article initially published, vesicular stomatitis virus was incorrectly identified as a double-stranded RNA virus. It should be identified as a single-stranded RNA virus throughout (and 'dsRNA' should be 'RNA' throughout the second paragraph and in the first sentence of the sixth paragraph and the seventh sentence of the seventh paragraph, and 'dsDNA' should be 'DNA' throughout). Also, the end of the second sentence of the second paragraph stated "TLR3 and TLR9 detect dsDNA viruses and dsRNA viruses, respectively". It should read as follows: "...TLR9 detects DNA viruses, and TLR3 and TLR7 detect RNA viruses." The correction notice posted on December 3 read "TLR3 and TLR9 detect RNA viruses" instead of "TLR3 and TLR7 detect RNA viruses." These errors have been corrected in the HTML and PDF versions of the article on 3 December 2014 and the correction notice on 10 April 2015.
References
Wang, et al. Nat. Immunol. 15, 1126–1133 (2014).
Kaczmarek, A., Vandenabeele, P. & Krysko, D.V. Immunity 38, 209–223 (2013).
Zhou, R., Yazdi, A.S., Menu, P. & Tschopp, J. Nature 469, 221–225 (2011).
Hornung, V. et al. Nat. Immunol. 9, 847–856 (2008).
Muñoz-Planillo, R. et al. Immunity 38, 1142–1153 (2013).
Knott, A.B., Perkins, G., Schwarzenbacher, R. & Bossy-Wetzel, E. Nat. Rev. Neurosci. 9, 505–518 (2008).
Mitoma, H. et al. Immunity 39, 123–135 (2013).
Franchi, L. et al. J. Immunol. 193, 4214–4222 (2014).
Subramanian, N., Natarajan, K., Clatworthy, M.R., Wang, Z. & Germain, R.N. Cell 153, 348–361 (2013).
Rajan, J.V., Rodriguez, D., Miao, E.A. & Aderem, A. J. Virol. 85, 4167–4172 (2011).
Allen, I.C. et al. Immunity 30, 556–565 (2009).
Thomas, P.G. et al. Immunity 30, 566–575 (2009).
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing interests
The authors declare no competing financial interests.
Rights and permissions
About this article
Cite this article
Rayamajhi, M., Miao, E. The RIP1-RIP3 complex initiates mitochondrial fission to fuel NLRP3. Nat Immunol 15, 1100–1102 (2014). https://doi.org/10.1038/ni.3030
Published:
Issue Date:
DOI: https://doi.org/10.1038/ni.3030
This article is cited by
-
Activated Drp1 regulates p62-mediated autophagic flux and aggravates inflammation in cerebral ischemia-reperfusion via the ROS-RIP1/RIP3-exosome axis
Military Medical Research (2022)
-
A surfactant polymer wound dressing protects human keratinocytes from inducible necroptosis
Scientific Reports (2021)
-
The kinase receptor-interacting protein 1 is required for inflammasome activation induced by endoplasmic reticulum stress
Cell Death & Disease (2018)
-
Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1
Scientific Reports (2017)
-
Expression of inflammation-related genes in the lung of BALB/c mice response to H7N9 influenza A virus with different pathogenicity
Medical Microbiology and Immunology (2016)