Reactive oxygen species generation in inflammatory signaling (ROS)

Reactive oxygen species (ROS) generation in inflammatory signaling refers to the production of highly reactive oxygen-containing molecules, such as superoxide and hydrogen peroxide, which serve as critical mediators in the immune response [1]. These species are primarily produced by enzymes like NADPH oxidases (NOX) and the mitochondrial electron transport chain in response to inflammatory stimuli like cytokines or pathogens [2]. While physiological levels of ROS are essential for cell signaling and host defense, their excessive or chronic production leads to oxidative stress, which triggers downstream pathways such as NF-kappaB and the NLRP3 inflammasome [3]. This sustained activation promotes the expression of pro-inflammatory genes, contributing to the pathogenesis of chronic diseases including rheumatoid arthritis, atherosclerosis, and neurodegeneration [4]. Therapeutic intervention typically involves the use of antioxidants to scavenge ROS or specific inhibitors to block ROS-producing enzymes like NOX2 [5]. However, targeting this process is challenging because ROS also play vital roles in normal cellular functions, such as wound healing and pathogen killing [6]. Consequently, non-selective inhibition can lead to impaired immunity or disrupted homeostatic signaling, a phenomenon often referred to as the antioxidant paradox [6].

Other names

Oxidative stress signalingRedox signalingPro-inflammatory ROS productionROS-mediated inflammationOxidative burst

Inhibition of ROS-producing enzymes (e.g., NADPH oxidase), direct scavenging of reactive species, or induction of endogenous antioxidant defense systems.