Scar tissue formation

Scar tissue formation, also known as cicatrization, is a fundamental biological process within the wound healing cascade where fibrous connective tissue replaces normal parenchymal tissue following injury [20, 23]. The process is characterized by three overlapping phases: inflammation, proliferation, and remodeling [11, 12]. During these stages, various cytokines and growth factors, most notably transforming growth factor-beta (TGF-beta), drive the activation of fibroblasts and their differentiation into contractile myofibroblasts [2, 6, 11]. These cells synthesize and deposit excessive amounts of extracellular matrix (ECM) proteins, primarily collagen types I and III, which provide structural support but lack the elasticity and specialized functions of the original tissue [20, 23]. When this process becomes dysregulated, it results in pathological outcomes such as hypertrophic scars, keloids, or systemic organ fibrosis [15, 21]. Therapeutic interventions aim to mitigate excessive scarring by targeting pro-fibrotic signaling pathways, inhibiting myofibroblast activity, or modulating mechanical tension within the wound environment using agents like verteporfin [8, 16, 22].

Other names

FibrosisCicatrizationDermal scarringPathological scarringHypertrophic scarringKeloid formationFibrogenesis

Inhibition of the TGF-beta/Smad signaling pathway to reduce fibroblast activation, suppression of cell proliferation using antimetabolites, disruption of mechanotransduction via YAP/TAZ inhibition to prevent tension-induced fibrogenesis, and enzymatic degradation of collagen fibers.