Keloid Disorder: Genetic Basis, Gene Expression Profiles, and Immunological Modulation of the Fibrotic Processes in the Skin

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Keloid disorder, a group of fibroproliferative skin disorders, is clinically comprised of keloids, hypertrophic scars, keloidalis nuchae, and acne keloidalis. The prototype of these disorders is keloids, which manifest as cutaneous lesions with excessive deposition of collagen following an initiating trauma of varying degrees. The principal cell type responsible for collagen accumulation is the myofibroblast, and its gene expression is modulated by a network of regulatory factors, including cytokines, growth factors, and noncoding RNA species. In addition, keloids harbor a number of inflammatory cells, including macrophages and mast cells, that interact with fibroblastic cells by direct contact or by paracrine actions. Transforming growth factor-β1/Smad signaling regulates the expression of genes encoding extracellular matrix proteins and also controls cell proliferation and apoptosis. A key profibrotic molecule is the fibronectin splice variant cellular fibronectin extracellular domain A (cFN-EDA), which interacts with a number of cell-surface integrins and TLR4, contributing to the modulation of gene expression by lesional fibroblasts. Collectively, these complex cellular interactions result in accumulation of collagen with clinical development and growth of keloid lesions. Understanding of the precise pathomechanistic details of keloid formation will provide targets for phar

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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