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. We explored 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 discussed. We aim to provide insights into the mechanisms of keloid formation and serve as a reference for developing future therapeutic strategies.
