Fibrotic tissue repair

Fibrotic tissue repair is a pathological biological process characterized by the excessive and persistent deposition of extracellular matrix (ECM) components, primarily collagen, in response to chronic tissue injury or inflammation [1, 3]. While normal tissue repair is a self-limiting homeostatic response, fibrotic repair becomes dysregulated, leading to the replacement of functional parenchyma with fibrous scar tissue and subsequent organ failure [1, 5]. This process is driven by the activation and persistence of myofibroblasts, which are often recruited or differentiated from local fibroblasts, pericytes, or epithelial cells under the influence of pro-fibrotic cytokines such as transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), and connective tissue growth factor (CTGF) [6, 7, 11]. Pathological fibrotic repair is a central feature of diverse chronic conditions, including idiopathic pulmonary fibrosis, liver cirrhosis, and chronic kidney disease [3, 15]. Therapeutic strategies targeting this process aim to inhibit the signaling cascades that promote myofibroblast activation, induce myofibroblast apoptosis, or directly interfere with ECM production and cross-linking [6, 11, 13]. Current clinical therapies, such as nintedanib and pirfenidone, act by blocking multiple tyrosine kinases or modulating cytokine production to slow the progression of fibrotic tissue accumulation [6, 14].

Other names

FibrosisFibrogenesisScarringTissue remodelingPathological wound healing

Inhibition of pro-fibrotic signaling pathways (e.g., TGF-beta, PDGF, FGF), modulation of myofibroblast activation/survival, and inhibition of extracellular matrix cross-linking enzymes such as lysyl oxidase-like 2 (LOXL2).