Systemic oxidative and inflammatory pathways

Systemic oxidative and inflammatory pathways represent a complex physiological network rather than a single molecular target. This network is primarily governed by the interplay between two key transcription factors: Nuclear factor erythroid 2-related factor 2 (Nrf2), which coordinates the antioxidant response, and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which drives pro-inflammatory gene expression (Wardyn et al., 2015, PubMed: 25529454). Under normal conditions, these pathways maintain cellular homeostasis; however, chronic activation of NF-κB and suppression of Nrf2 are linked to the pathogenesis of various diseases, including neurodegeneration, cardiovascular disorders, and chronic inflammation (Sivandzade et al., 2019, PubMed: 30849441). Pharmacological intervention typically involves small molecules like Bardoxolone methyl or Dimethyl fumarate that stabilize Nrf2 to enhance cytoprotective mechanisms or inhibit the IKK complex to prevent NF-κB activation (Liby & Sporn, 2012, PubMed: 22508260). Because this 'target' encompasses broad systemic processes, therapeutic agents often face challenges regarding specificity and the risk of disrupting essential physiological signaling.

Other names

Oxidative stress signalingInflammatory signaling pathwaysNrf2-NF-κB axisRedox-inflammatory network

Modulation of cellular redox status and inflammatory gene expression via the activation of Nrf2-mediated antioxidant responses and the inhibition of NF-κB-mediated pro-inflammatory signaling.