Inflammatory and oxidative stress pathways

Inflammatory and oxidative stress pathways comprise a complex, bidirectional network of signaling events that regulate cellular responses to internal and external stressors. These pathways involve the production of reactive oxygen species (ROS) and the activation of pro-inflammatory transcription factors like NF-κB, which in turn promote the expression of cytokines and chemokines (Hussain et al., 2016). Chronic activation of these pathways creates a feedback loop where oxidative damage triggers inflammatory responses, further exacerbating tissue injury. This vicious cycle is a fundamental driver in the pathogenesis of chronic conditions such as atherosclerosis, type 2 diabetes, and neurodegenerative disorders (Reuter et al., 2010). Therapeutic intervention typically involves modulating key nodes within these pathways, such as activating the Nrf2 antioxidant response or inhibiting pro-inflammatory enzymes. Drugs like dimethyl fumarate and bardoxolone methyl are designed to shift the cellular environment from a pro-inflammatory/oxidative state to a cytoprotective one. However, because this term describes a broad biological process involving hundreds of distinct proteins rather than a single molecule, it is classified as a pathway rather than a discrete therapeutic target.

Other names

Oxidative-inflammatory axisRedox-inflammatory signalingInflammation-oxidative stress cascade

Modulation of redox-sensitive transcription factors (e.g., Nrf2 activation, NF-κB inhibition), scavenging of reactive oxygen species, and suppression of pro-inflammatory cytokine production (Hussain et al., 2016; StatPearls, 2023).