Tissue fibrosis

Tissue fibrosis is a chronic pathological process characterized by the excessive and persistent accumulation of extracellular matrix (ECM) components, primarily collagen, within organs and tissues (Wynn, 2008). It typically results from a dysregulated wound-healing response following chronic inflammation or repeated tissue injury, where the body's repair mechanisms fail to resolve, leading to the replacement of functional parenchyma with permanent scar tissue (StatPearls, 2023). At the molecular level, this process is driven by the activation and proliferation of myofibroblasts, which are triggered by various signaling pathways, most notably the Transforming growth factor-beta (TGF-beta) and Platelet-derived growth factor (PDGF) cascades (NIH, 2013; PubMed, 2012). Fibrosis is a central feature of many progressive and life-threatening diseases, including idiopathic pulmonary fibrosis, liver cirrhosis, and chronic kidney disease, eventually leading to organ failure. While 'Tissue fibrosis' refers to a disease state rather than a single molecular receptor or enzyme, therapeutic interventions target the specific molecular mediators and signaling hubs that orchestrate this complex biological response. Current drug development efforts focus on small molecules and biologics that can arrest or reverse the deposition of ECM to preserve organ architecture and function (NIH, 2021).

Other names

Fibrotic diseaseOrgan fibrosisPathological scarringFibroplasiaSclerosis

Anti-fibrotic agents generally function by inhibiting tyrosine kinase receptors involved in growth factor signaling (such as PDGFR, FGFR, and VEGFR) or by neutralizing pro-fibrotic cytokines like Transforming growth factor-beta (TGF-beta) and Connective tissue growth factor (CTGF) to prevent myofibroblast differentiation and extracellular matrix deposition (Wynn, 2008; PubMed, 2012; StatPearls, 2023).