Mitochondrial reactive oxygen species drive proinflammatory cytokine production
Open Access
- 28 February 2011
- journal article
- review article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 208 (3), 417-420
- https://doi.org/10.1084/jem.20110367
Abstract
High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn’s disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proinflammatory cytokine production. New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways.Keywords
This publication has 17 references indexed in Scilit:
- Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS)The Journal of Experimental Medicine, 2011
- The inflammasomes: mechanisms of activation and functionCurrent Opinion in Immunology, 2010
- The Inflammasomes: Guardians of the BodyAnnual Review of Immunology, 2009
- Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and SilicaScience, 2008
- Reactive Oxygen Species Promote TNFα-Induced Death and Sustained JNK Activation by Inhibiting MAP Kinase PhosphatasesCell, 2005
- Cytokine-Based Therapies for Crohn's Disease — New ParadigmsThe New England Journal of Medicine, 2004
- Mitochondrial Respiratory-Chain DiseasesThe New England Journal of Medicine, 2003
- Post-transcriptional regulation of tumour necrosis factor alpha productionAnnals Of The Rheumatic Diseases, 2000
- Germline Mutations in the Extracellular Domains of the 55 kDa TNF Receptor, TNFR1, Define a Family of Dominantly Inherited Autoinflammatory SyndromesCell, 1999
- Reactive oxygen species activity and lipid peroxidation inHelicobacter pylori associated gastritis: relation to gastric mucosal ascorbic acid concentrations and effect of H pylori eradicationGut, 1998