Fibrosis pathways

"Fibrosis pathways" refers to the diverse network of molecular and cellular signaling cascades that drive the excessive deposition of extracellular matrix and scar tissue in response to persistent tissue injury, chronic inflammation, or perturbations in wound healing. Key pathways include transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF), JAK/STAT, Wnt/β-catenin, Notch, and Hippo-YAP/TAZ, as well as integrin-mediated mechanotransduction. These pathways coordinate the activation of myofibroblasts, epithelial-mesenchymal transition, immune cell recruitment, and persistent secretion of pro-fibrotic mediators, all contributing to tissue stiffening and organ dysfunction. Because these are pathways—not single molecules or receptors—'fibrosis pathways' as a term should not be used as a canonical drug target or receptor. Instead, individual components of these pathways (such as TGF-β receptor, PDGF receptor, or JAK kinases) serve as the actual druggable targets in anti-fibrotic therapy development[1][2][3][4][5][6]. Summary: - "Fibrosis pathways" is not a specific molecule or receptor but a category of signaling pathways. - It is not considered a canonical therapeutic target and is not suitable for structured target databases as a unique entity. - For actionable information, identify the specific molecular target within the relevant fibrosis pathway (e.g., "Transforming growth factor-beta receptor 1").

Other names

Fibrotic pathwaysPathways in fibrosisPro-fibrotic signaling pathwaysFibrogenic pathways

Inhibition of TGF-β signaling (reduces profibrotic gene expression); Inhibition of PDGF, FGF, and VEGF signaling (suppresses fibroblast proliferation); Inhibition of JAK/STAT pathway (reduces inflammation and fibrogenesis); Modulation of Notch, Wnt/β-catenin, and Hippo-YAP/TAZ pathways