氧化应激
血管生成
伤口愈合
细胞生物学
癌症研究
内皮干细胞
药理学
内分泌学
生物
免疫学
体外
生物化学
作者
Hainan Li,Liping Xu,Sai Pranathi Meda Venkata,Morgan Minjares,Hassan Melhem,Anjaneyulu Kowluru,Jan Hendrik Niess,Graeme Milligan,Jie‐Mei Wang
出处
期刊:Diabetes
[American Diabetes Association]
日期:2025-04-23
卷期号:74 (7): 1233-1246
摘要
Endothelial cell dysfunction is a crucial feature of diabetic wound healing. The underlying molecular mechanisms are poorly understood. We investigated how G protein-coupled receptor 35 (GPR35) inhibition accelerates diabetic wound healing. We found that GPR35 modulated endothelial cell behavior in vitro and identified oxidative stress responsive 1 as its target. Inhibiting GPR35 rescued the healing process in animals with hyperglycemia. This study uncovers novel molecular mechanisms underlying the benefit of GPR35 inhibition on endothelial cell angiogenesis and provides proof-of-concept evidence for therapeutic strategies targeting GPR35 in the endothelium as a potential therapy for diabetic wound care.
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