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Pro-inflammatory macrophage differentiation is the process by which monocytes or precursor macrophages are driven to adopt a pro-inflammatory (M1) phenotype. M1 macrophages play a central role in initiating and sustaining inflammatory responses, particularly during infection, tissue injury, and certain chronic diseases. This process is characterized by specific inducing factors (GM-CSF, IFN-γ, LPS), surface markers (iNOS, CD147), a pro-inflammatory cytokine profile (TNF-α, IL-6, IL-12, IL-23), activation of intracellular signaling pathways (JAK2–STAT5, NF-kB, PI3K/Akt, MAPKs), and a metabolic shift towards glycolysis. Targeting M1 macrophage differentiation represents a therapeutic strategy for managing inflammatory diseases.
Targeting upstream signaling pathways (JAK/STAT, NF-kB, PI3K/Akt, MAPK) or metabolic pathways (glycolysis) to inhibit M1 macrophage polarization or promote M2 polarization.
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