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Significance GPR39 is an orphan GPR whose physiological ligand and intracellular pathways in ECs remain poorly characterized. Our data indicate that inhibition of GPR39 protects EC functions by enhancing SHH… Click to show full abstract
Significance GPR39 is an orphan GPR whose physiological ligand and intracellular pathways in ECs remain poorly characterized. Our data indicate that inhibition of GPR39 protects EC functions by enhancing SHH signaling in aortic ECs. Understanding the potential cross-talk between GPR39 activation and SHH signaling in hyperglycemia may form the basis for developing therapeutic approaches to target cardiovascular complications in diabetic patients. Our studies also revealed that genetic ablation of GPR39 significantly improves revascularization after ischemia in vivo in a type 2 diabetic mouse model. Our studies open an avenue to preserving endothelial function and vascular health by targeting GPR39. The development of pharmacological or genetic agents to block GPR39 in ECs may be a fruitful area of future research.
Journal Title: Proceedings of the National Academy of Sciences of the United States of America
Year Published: 2022
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