Fibrosis inhibition

"Fibrosis inhibition" describes a therapeutic approach aiming to prevent, reduce, or reverse pathological fibrotic tissue remodeling in a range of chronic diseases by targeting molecules and pathways responsible for fibroblast activation, extracellular matrix (ECM) deposition, and cytokine signaling. Several drugs target receptors such as TGF-β, PDGF, or growth factor signaling, and others inhibit downstream intracellular or extracellular mediators involved in fibrosis progression[1][2][3][4][5][6][7]. Direct targets include receptor tyrosine kinases (FGFR, VEGFR, PDGFR), nuclear receptors (FXR), cytokines (TNF, TGF-β, interleukins), and recently discovered pathways (Notch, Hedgehog, etc.). Precision in drug targeting is critical, as broad inhibition may lead to adverse effects or paradoxical worsening of disease[3][4]. **Note:** "Fibrosis inhibition" is not a molecular entity or receptor but refers to a set of therapeutic interventions. For structured data extraction, the actual drug targets should be referenced (e.g., TGF-β receptor, PDGF receptor, FGFR, FXR) rather than this umbrella term.

Other names

Anti-fibrotic therapyAntifibrotic strategyFibrosis blockadeFibrosis preventionAnti-fibrosis drugs

Inhibition of cytokine signaling (e.g., TGF-β, PDGF, CTGF); Blockade of receptor tyrosine kinases (e.g. FGFR, VEGFR, PDGFR); Suppression of fibroblast activation and differentiation; Inhibition of growth factors and interleukins; Modulation of extracellular matrix synthesis/degradation; Targeting hepatic stellate cells (HSCs)