Inflammatory processes secondary to oxidative stress

Inflammatory processes secondary to oxidative stress represent a complex pathophysiological state rather than a single molecular target. This condition occurs when an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defenses triggers chronic inflammatory signaling (Sies et al., 2017). ROS act as secondary messengers that 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 (Hussain et al., 2016). This relationship is bidirectional, as activated inflammatory cells release further ROS, creating a self-perpetuating feedback loop that exacerbates tissue damage and contributes to the progression of chronic diseases such as atherosclerosis and neurodegeneration (Reuter et al., 2010). While the process itself is not a discrete drug target, therapeutic strategies focus on specific nodes within this cascade, such as the Nrf2-Keap1 pathway to enhance antioxidant capacity or the inhibition of ROS-generating enzymes like NADPH oxidase (NOX). Understanding this interplay is critical for developing interventions that can break the cycle of oxidative damage and chronic inflammation.

Other names

Oxidative stress-induced inflammationRedox-mediated inflammationROS-driven inflammationOxidative-inflammatory cascade

Drugs typically modulate this process by scavenging reactive oxygen species (ROS), inducing endogenous antioxidant enzymes via the Nrf2/ARE pathway, or inhibiting pro-inflammatory signaling cascades such as the NF-kappaB pathway.