Zhijin Li, PhD in Plastic and Reconstructive Surgery from Peking Union Medical College Hospital, Chinese Academy of Medical Sciences; currently serving as a clinical postdoctoral fellow at the same institution. Research interests include skin aging, facial rejuvenation, scarring and skin fibrosis, and adipose tissue regulation. Published over 10 SCI papers as first author or co-first author in international journals such as Plastic and Reconstructive Surgery (PRS), Journal of Investigative Dermatology (JID), and Aesthetic Surgery Journal (ASJ). Participated in academic exchange and training at Nippon Medical School in Japan.
Abstract submitted for the 5th International Keloid Symposium
Title: Unraveling the Vascular Tapestry: Endothelial Dysfunction in Keloid Formation and Therapeutic Insights
AUTHORS: Zhijin Li1,Junxian Wen1,2, Yingrou Tan2, 3, Hong Liang Tey2,4, Nanze Yu1,5, Xiao Long1, Xiaojun Wang1
AUTHORS’ AFFILIATIONS:
1 Department of Plastic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
2 National Skin Centre, Singapore.
3 Skin Research Institute of Singapore, Singapore.
4 Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore.
5 Department of International Medical Service, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Background: For keloids, 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.
Methods: Four databases, including Medline, Embase, Web of Science, and the Cochrane Library, were searched from their inception dates to November 2024. The search was restricted to English-language publications to maintain consistency and focus. The search strategy included terms such as “Keloid”, “Blood Vessels”, “Microcirculation”, and “Endothelium” to identify studies exploring vascular and endothelial mechanisms in keloid pathogenesis and treatment. Additionally, references cited in the selected articles were screened for further studies of interest to ensure comprehensive coverage.
Results: This review explores the direct and indirect mechanisms of ED in keloid progression, including endothelial-to-mesenchymal transition (EndoMT), inflammation, immune cell crosstalk, and hypoxia. Additionally, 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 endothelial dysfunction. It aims to provide insights into the mechanisms of keloid formation and serve as a reference for developing future therapeutic strategies.
Conclusion: Keloids, which are characterized by vascular irregularities and increased blood vessel density, exhibit imbalances in proangiogenic and antiangiogenic factors. These deviations in vascular architecture and the increase in blood vessel density contribute to a hypoxic microenvironment the mediates angiogenesis and collagen synthesis. Endothelial dysfunction in keloids involves a complex interplay between imbalanced pro-/antiangiogenic factors and endothelial dynamics. ED directly impacts endothelial-to-mesenchymal transition and indirectly supports inflammation and immune cell crosstalk, thereby promoting fibrosis in keloids. Therapeutic interventions targeting ED include anti-VEGF drugs, radiotherapy, hyperbaric oxygen therapy, compression therapy, and laser treatments. In the future, continued exploration of the specific mechanisms underlying vascular endothelial dysfunction and the targeted development of effective keloid treatment methods will be crucial.
