Fibrosis-associated cellular pathways

Fibrosis-associated cellular pathways represent a complex network of signaling cascades that drive the excessive accumulation of extracellular matrix (ECM) proteins, leading to tissue scarring and organ failure (Source: NIH, StatPearls). The most prominent of these is the Transforming Growth Factor-beta (TGF-beta) pathway, which promotes the differentiation of fibroblasts into contractile myofibroblasts (Source: PubMed, PMID: 30659449). Other critical pathways include the Platelet-Derived Growth Factor (PDGF), Wnt/beta-catenin, and Hippo signaling pathways, all of which contribute to cell proliferation and ECM synthesis (Source: Nature Reviews Disease Primers). In chronic diseases such as idiopathic pulmonary fibrosis, liver cirrhosis, and systemic sclerosis, these pathways become dysregulated and persistently active (Source: Mayo Clinic). Therapeutic strategies aim to inhibit these pathways using small molecules like Nintedanib, which targets multiple tyrosine kinases, or Pirfenidone, which has broad anti-fibrotic and anti-inflammatory effects (Source: FDA, 2014). However, because these pathways are also essential for normal wound healing and physiological homeostasis, systemic inhibition can lead to significant safety concerns and side effects (Source: Journal of Clinical Investigation).

Other names

Fibrotic signaling pathwaysPro-fibrotic pathwaysFibrogenesis pathways

Inhibition of pro-fibrotic signaling cascades, including TGF-beta, PDGF, and VEGF pathways, to reduce myofibroblast activation and extracellular matrix deposition (Source: PubMed, PMC4292109; FDA Labeling).