Redox regulation of inflammation: old elements, a new story
- PMID: 25171147
- DOI: 10.1002/med.21330
Redox regulation of inflammation: old elements, a new story
Abstract
Inflammation is an essential immune response characterized by pain, swelling, redness, heat, and impaired function. A controlled acute inflammatory response is necessary to fight off infection and overcome injury. However, if the inflammatory process persists and enters into the chronic state, it can lead to local and systemic deleterious effects counterproductive to healing and instead constitutes a new pathology. Typically, inflamed tissues are associated with an elevated level of reactive species (reactive oxygen species (ROS)/reactive nitrogen species (RNS)). These ROS/RNS are generated during the respiratory burst of immune cells and are important factors in defense against invading pathogens. Additionally, reactive species are now known to trigger oxidative/nitrosative modifications of biomolecules. While most of these modifications lead to irreparable damage, some are subtle and fully reversible. The reversible modifications can initiate signaling cascades known as "redox signaling." This redox signaling tightly modulates the inflammatory response. Thus, understanding the complex role of ROS/RNS-induced redox signaling in inflammation will assist in the design of relevant therapeutic intervention strategies for inflammation-associated diseases. This review will highlight the impact of oxidative stress and redox signaling on inflammation and inflammation-associated diseases, with a focus on redox modifications of inflammation-related proteins.
Keywords: HMGB1; NF-κB; ROS/RNS; inflammation; redox modifications.
© 2014 Wiley Periodicals, Inc.
Similar articles
-
L-gamma-Glutamyl-L-cysteinyl-glycine (glutathione; GSH) and GSH-related enzymes in the regulation of pro- and anti-inflammatory cytokines: a signaling transcriptional scenario for redox(y) immunologic sensor(s)?Mol Immunol. 2005 May;42(9):987-1014. doi: 10.1016/j.molimm.2004.09.029. Epub 2004 Nov 23. Mol Immunol. 2005. PMID: 15829290 Review.
-
Quantitative redox proteomics: the NOxICAT method.Methods Mol Biol. 2012;893:387-403. doi: 10.1007/978-1-61779-885-6_24. Methods Mol Biol. 2012. PMID: 22665313
-
Redox proteomics: basic principles and future perspectives for the detection of protein oxidation in plants.J Exp Bot. 2008;59(14):3781-801. doi: 10.1093/jxb/ern252. J Exp Bot. 2008. PMID: 18977746 Review.
-
Inflammation and lung cancer: roles of reactive oxygen/nitrogen species.J Toxicol Environ Health B Crit Rev. 2008 Jan;11(1):1-15. doi: 10.1080/10937400701436460. J Toxicol Environ Health B Crit Rev. 2008. PMID: 18176884 Review.
-
Gene regulation by melatonin linked to epigenetic phenomena.Gene. 2012 Jul 15;503(1):1-11. doi: 10.1016/j.gene.2012.04.040. Epub 2012 May 1. Gene. 2012. PMID: 22569208 Review.
Cited by
-
The biomedical applications of nanozymes in orthopaedics based on regulating reactive oxygen species.J Nanobiotechnology. 2024 Sep 16;22(1):569. doi: 10.1186/s12951-024-02844-3. J Nanobiotechnology. 2024. PMID: 39285458 Free PMC article. Review.
-
Breaking the vicious loop between inflammation, oxidative stress and coagulation, a novel anti-thrombus insight of nattokinase by inhibiting LPS-induced inflammation and oxidative stress.Redox Biol. 2020 May;32:101500. doi: 10.1016/j.redox.2020.101500. Epub 2020 Mar 11. Redox Biol. 2020. PMID: 32193146 Free PMC article.
-
Ischemic modified albumin as a new biomarker in predicting oxidative stress in alopecia areata.Turk J Med Sci. 2019 Feb 11;49(1):129-138. doi: 10.3906/sag-1708-35. Turk J Med Sci. 2019. PMID: 30762322 Free PMC article.
-
Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases.Redox Biol. 2020 Jul;34:101506. doi: 10.1016/j.redox.2020.101506. Epub 2020 Apr 20. Redox Biol. 2020. PMID: 32371009 Free PMC article. Review.
-
Inhibition of NLRP3 Inflammasome Prevents LPS-Induced Inflammatory Hyperalgesia in Mice: Contribution of NF-κB, Caspase-1/11, ASC, NOX, and NOS Isoforms.Inflammation. 2017 Apr;40(2):366-386. doi: 10.1007/s10753-016-0483-3. Inflammation. 2017. PMID: 27924425
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources