Reactive oxygen species-dependent inflammatory signaling pathway (ROS-inflammatory signaling)

Reactive oxygen species (ROS)-dependent inflammatory signaling is a complex biological process where oxygen-derived free radicals and non-radicals act as secondary messengers to initiate and sustain inflammatory responses. ROS are primarily generated by the mitochondrial respiratory chain and enzymatic complexes such as NADPH oxidases (NOX) in response to various stimuli, including pathogens and tissue injury (Mittler, 2017; PubMed: 28239127). These molecules activate redox-sensitive transcription factors, most notably Nuclear Factor-kappa B (NF-κB), which orchestrates the expression of pro-inflammatory cytokines, chemokines, and adhesion molecules (Morgan & Liu, 2011; PubMed: 21233854). Furthermore, ROS are critical for the assembly and activation of the NLRP3 inflammasome, leading to the maturation of interleukin-1 beta (IL-1β) (Tschopp & Schroder, 2010; PubMed: 20303873). Dysregulation of this pathway leads to chronic oxidative stress, a hallmark of numerous pathologies including atherosclerosis, neurodegenerative disorders, and cancer. Pharmacological intervention typically targets specific nodes within this pathway, such as inhibiting NOX enzymes or activating the Nrf2-mediated antioxidant defense system to restore redox homeostasis (Ma, 2013; PubMed: 23286283).

Other names

ROS-mediated inflammationOxidative stress-induced inflammatory signalingRedox-sensitive inflammatory signalingROS-NF-kappaB axisROS-NLRP3 signaling

Modulation of redox homeostasis through the scavenging of reactive oxygen species, inhibition of ROS-generating enzymes such as NADPH oxidase (NOX), or the pharmacological activation of the Nrf2-mediated antioxidant response to suppress downstream pro-inflammatory cascades including the NF-kappaB pathway and the NLRP3 inflammasome.