Endothelial Dysfunction in Keloid Formation and Therapeutic Insights

Keloids are benign fibroproliferative tumors that cause significant physical and mental morbidity owing to their disfiguring appearance, chronic symptoms, and resistance to treatment. Although fibroblast hyperproliferation and excessive extracellular matrix deposition have been extensively studied, less attention has been paid to the role of vascular dysregulation and endothelial dysfunction (ED) in keloid pathogenesis. Emerging evidence highlights abnormal angiogenesis, vascular irregularities, and endothelial injury as critical drivers of fibrosis in keloids. This review explores the direct and indirect mechanisms of ED in keloid progression, including endothelial-to-mesenchymal transition, inflammation, immune cell crosstalk, and hypoxia. In addition, various treatment strategies targeting angiogenesis and ED, such as drugs, radiotherapy, hyperbaric oxygen therapy, compression, and laser treatments, are comprehensively reviewed. This review explores keloids through the lens of vasculature and endothelium, emphasizing the critical roles of vascular dysregulation and ED. It aims to provide insights into the mechanisms of keloid formation and serve as a reference for developing future therapeutic strategies.