title: 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.
authors.affiliation: State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China; Department of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, P.R. China.
authors.forename: Yunlong
authors.initials: Y
authors.lastname: Lei
authors.forename: Kui
authors.initials: K
authors.lastname: Wang
authors.forename: Longfei
authors.initials: L
authors.lastname: Deng
authors.forename: Yi
authors.initials: Y
authors.lastname: Chen
authors.forename: Edouard C
authors.initials: EC
authors.lastname: Nice
authors.forename: Canhua
authors.initials: C
authors.lastname: Huang
mesh_terms: D000818:Animals; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology*; D046911:Macromolecular Substances / Q000378:metabolism; D008954:Models, Biological; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D046911:Macromolecular Substances; D017382:Reactive Oxygen Species
keywords: HMGB1; NF-κB; ROS/RNS; inflammation; redox modifications