Article thumbnail

Mitochondrial reactive oxygen species drive proinflammatory cytokine production

By Edwina Naik and Vishva M. Dixit

Abstract

Recent work indicates that mitochondrial ROS act via several pathways to elicit proinflammatory cytokines in human and mouse cells

Topics: Minireview
Publisher: The Rockefeller University Press
OAI identifier: oai:pubmedcentral.nih.gov:3058577
Provided by: PubMed Central

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.

Suggested articles

Citations

  1. (2011). Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome.
  2. (2010). Concerted action of wildtype and mutant TNF receptors enhances inflam mation in TNF receptor 1associated peri odic fever syndrome.
  3. (2004). Cytokinebased therapies for Crohn’s disease—new paradigms.
  4. (2007). Defective mitochondrial bio genesis: a hallmark of the high cardiovascular risk in the metabolic syndrome?
  5. (1999). Germline muta tions in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a fam ily of dominantly inherited autoinflamma tory syndromes.
  6. Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica.
  7. (2011). Mitochondrial reac tive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1associated periodic syndrome (TRAPS).
  8. (2000). Posttranscriptional regulation of tumour necrosis factor alpha production.
  9. (1998). Reactive oxygen species activity and lipid peroxidation in Helicobacter pylori associated gastritis: relation to gastric mucosal ascorbic acid concentrations and ef fect of H pylori eradication.
  10. (2005). Reactive oxygen species promote TNFalphainduced death and sustained JNK activation by inhibiting MAP kinase phosphatases.