General cellular oxidative and inflammatory pathways

General cellular oxidative and inflammatory pathways represent a complex, integrated network of biochemical processes that respond to internal and external stressors to maintain cellular homeostasis [1]. These pathways are characterized by the production of reactive oxygen species (ROS) and the activation of transcription factors such as Nuclear Factor-kappa B (NF-κB) and Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2), which regulate the expression of genes involved in the immune response and antioxidant defense [2]. While transient activation is necessary for physiological processes like wound healing and pathogen clearance, chronic dysregulation leads to persistent oxidative stress and systemic inflammation [3]. This chronic state is a fundamental driver in the pathogenesis of diverse conditions, including cardiovascular disease, neurodegeneration, and cancer [1]. Therapeutic interventions targeting these pathways range from non-steroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenases to Nrf2 activators that bolster endogenous antioxidant capacity [2,3]. However, because these pathways are integral to normal cellular signaling and defense, their broad modulation poses significant challenges regarding specificity and the risk of adverse effects such as immunosuppression or impaired redox signaling [2].

Other names

Oxidative stress pathwaysInflammatory signaling cascadesRedox signalingPro-inflammatory pathways

Drugs targeting these pathways act through several mechanisms, including the inhibition of cyclooxygenase (COX) enzymes to reduce prostaglandin synthesis, the activation of the Nrf2-Keap1 pathway to enhance endogenous antioxidant gene expression, the inhibition of the NF-κB signaling cascade to suppress pro-inflammatory cytokine production, and the direct scavenging of reactive oxygen species (ROS) [1,2,3].