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Oxidative stress and inflammation-related proteins represent a diverse functional class of molecules that mediate the cellular response to oxidative damage and inflammatory stimuli. This group encompasses transcription factors such as Nuclear factor erythroid 2-related factor 2 (Nrf2) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which act as master regulators of antioxidant and pro-inflammatory genes, respectively (Hussain et al., 2016, PubMed). It also includes enzymes like Cyclooxygenase-2 (COX-2) and various Superoxide dismutases (SOD), as well as signaling cytokines like Tumor necrosis factor-alpha (TNF-α) (Wardyn et al., 2015, PubMed). These proteins are central to the pathogenesis of chronic diseases, where a persistent imbalance between reactive oxygen species (ROS) production and antioxidant defense leads to tissue damage and chronic inflammation (Marrocco et al., 2017, PubMed). Therapeutic intervention typically involves targeting specific nodes within these pathways, such as using Nrf2 activators to boost endogenous defenses or TNF inhibitors to suppress systemic inflammation (NIH, 2023). Because this term describes a broad biological category rather than a single protein or receptor, it is not considered a discrete therapeutic target in drug discovery and is marked as incorrect for structured target identification.
Modulation of redox-sensitive transcription factors (e.g., Nrf2 activation, NF-kB inhibition), enzymatic inhibition of inflammatory mediators (e.g., COX-2 inhibition), and direct neutralization of pro-inflammatory cytokines.
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