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Multiple inflammatory and oxidative stress pathways refer to a complex, interconnected network of signaling cascades, such as NF-κB, Nrf2-Keap1, and MAPK, that coordinate the cellular response to environmental and endogenous stressors [1, 3]. These pathways are characterized by the generation of reactive oxygen species (ROS) and the subsequent activation of pro-inflammatory cytokines, creating a self-amplifying cycle often implicated in the pathogenesis of chronic diseases like diabetes, neurodegeneration, and cardiovascular disorders [2, 7]. In pharmacological research, this term is frequently used to describe the pleiotropic effects of bioactive compounds, such as curcumin or resveratrol, which modulate several nodes within these networks simultaneously rather than binding to a single discrete receptor [4, 5]. Because this designation encompasses a wide array of enzymes, transcription factors, and signaling molecules, it does not represent a single, specific therapeutic target [8]. Consequently, drugs associated with these pathways often face challenges regarding target specificity and the potential for disrupting essential physiological redox signaling [10].
Modulation of broad signaling networks including NF-κB, Nrf2-Keap1, and MAPK cascades to reduce pro-inflammatory cytokine production and enhance endogenous antioxidant defenses.
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