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“Pro-inflammatory and profibrotic pathways” refers to broad networks of **cytokines, growth factors, and intracellular signaling** that orchestrate both inflammatory and fibrogenic responses in tissues. Central mediators include **transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α), interleukins (IL-1β, IL-6, IL-13), and profibrotic factors such as connective tissue growth factor (CTGF)**[1][2][3][4][5]. These pathways converge on key intracellular cascades—such as Smad, JAK/STAT, PI3K/AKT/mTOR, and JNK signaling—that control the activation of fibroblasts, differentiation to myofibroblasts, and excessive deposition of extracellular matrix (fibrosis)[1][2][6][7]. Dysregulation leads to chronic inflammation, pathological fibrosis, organ failure, and contributes to cancer. Because they are essential to normal wound healing, therapeutic interventions require precise targeting to avoid deleterious side effects[6].
Modulation of cytokine signaling Inhibition of growth factor receptors Suppression of downstream signaling cascades (e.g., JAK/STAT, Smad, PI3K/AKT, JNK) Attenuation of fibroblast activation and ECM production
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