TEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblasts

Hong, Yi-KaiYi-KaiHongLin, Yu-ChenYu-ChenLinCheng, Tsung-LinTsung-LinChengLai, Chao-HanChao-HanLaiChang, Yi-HanYi-HanChangHuang, Yu-LunYu-LunHuangHung, Chia-YiChia-YiHungWu, Chen-HanChen-HanWuHung, Kuo-ShuKuo-ShuHungKu, Ya-ChuYa-ChuKuHo, Yen-TingYen-TingHoTang, Ming-JerMing-JerTangSHU-WHA LINShi, Guey-YuehGuey-YuehShiMcGrath, John AJohn AMcGrathWu, Hua-LinHua-LinWuHsu, Chao-KaiChao-KaiHsu2024-03-082024-03-082024-01-2310217770https://scholars.lib.ntu.edu.tw/handle/123456789/640721Pathologic scars, including keloids and hypertrophic scars, represent a common form of exaggerated cutaneous scarring that is difficult to prevent or treat effectively. Additionally, the pathobiology of pathologic scars remains poorly understood. We aim at investigating the impact of TEM1 (also known as endosialin or CD248), which is a glycosylated type I transmembrane protein, on development of pathologic scars.enFibroblast activation; Hypertrophic scar; Keloid; TEM1/endosialin/CD248; TGF-βTEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblastsjournal article10.1186/s12929-024-01001-0382540972-s2.0-85182859730https://api.elsevier.com/content/abstract/scopus_id/85182859730