Epithelial-mesenchymal transition in keloid tissue

Fibroblasts at the wound site are recognized as the primary drivers of scar formation. They differentiate into myofibroblasts, the key mediators of fibrosis, which are responsible for collagen deposition and wound contraction. Repair processes cease when epithelialization is completed in normal wounds, whereas in keloid wounds, they may continue and result in excessive accumulation of unorganized extracellular matrix, forming problematic scars. In addition to resident mesenchymal cells, fibroblasts and myofibroblasts are thought to be derived from multiple sources, including epithelialmesenchymal transition (EMT) [1]. During this process, epithelial cells experience intercellular and intracellular changes, including dissociation of junctional complexes, loss of apical-basolateral polarity, and repression of epithelial markers. As a IMAGES