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Proinflammatory markers are a diverse group of signaling molecules, including cytokines, chemokines, enzymes, and acute-phase proteins, that initiate and sustain the host's inflammatory response to injury, infection, or stress (MDPI, 2024). Major members such as Tumor necrosis factor-alpha (TNF-α), Interleukin-1 (IL-1), and Interleukin-6 (IL-6) act as primary mediators that activate cellular pathways like NF-κB and JAK/STAT, leading to the recruitment of immune cells and the further production of inflammatory factors (Frontiers, 2025; PMC, 2025). While essential for acute defense and tissue repair, the chronic or dysregulated expression of these markers is a defining feature of many pathological states, including rheumatoid arthritis, inflammatory bowel disease, and neurodegenerative disorders such as Alzheimer's disease (Frontiers, 2025; ResearchGate, 2025). Therapeutic management involves the use of biologics to sequester specific cytokines, receptor antagonists to prevent signal transduction, and small molecule inhibitors that target upstream regulatory enzymes like cyclooxygenase-2 (COX-2) (MDPI, 2024). Monitoring these markers in serum or tissue serves as a critical clinical tool for assessing disease severity and evaluating the effectiveness of anti-inflammatory interventions (medRxiv, 2025; PMC, 2025).
Drugs targeting proinflammatory markers typically function by neutralizing circulating mediators using monoclonal antibodies, blocking cognitive receptors through receptor antagonism, or inhibiting the intracellular signaling pathways (e.g., JAK/STAT) and enzymatic activities (e.g., COX-2) responsible for their synthesis and pathological effects (MDPI, 2024; ResearchGate, 2025).
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