{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hua D"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["1441"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11538459"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["The endothelium-dependent vascular injury, a primary pathological feature of angiotensin II (Ang II)-induced hypertension. This study aimed to explore the role and underlying mechanisms of G protein-coupled receptor 39 (GPR39) in the pathogenesis of Ang II-induced hypertension. For in vivo studies, GPR39 knockout (KO) mice (C57BL/6 J, male) were generated and administered Ang II for 4 weeks. GPR39 expression was upregulated in the aorta of hypertensive patients and mice. The ablation of GPR39 mitigated vascular fibrosis, augmented endothelium-dependent vasodilation, and inhibited endothelial inflammation, oxidative stress, and apoptosis in mice. Additionally, GPR39 KO decreased NOD-like receptor protein 3 (Nlrp3) gene expression in Ang II-stimulated endothelial cells. Notably, Nlrp3 activa"],"journal":["Communications biology"],"pubmed_title":["Targeting GPR39 in structure-based drug discovery reduces Ang II-induced hypertension."],"pmcid":["PMC11538459"],"funding_grant_id":["82070438"],"pubmed_authors":["Sheng Y","Tang L","Cao X","Hua D","Liu M","Huang W","Li P","Xie Q","Xu W","Zhang Q","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"Targeting GPR39 in structure-based drug discovery reduces Ang II-induced hypertension.","description":"The endothelium-dependent vascular injury, a primary pathological feature of angiotensin II (Ang II)-induced hypertension. This study aimed to explore the role and underlying mechanisms of G protein-coupled receptor 39 (GPR39) in the pathogenesis of Ang II-induced hypertension. For in vivo studies, GPR39 knockout (KO) mice (C57BL/6 J, male) were generated and administered Ang II for 4 weeks. GPR39 expression was upregulated in the aorta of hypertensive patients and mice. The ablation of GPR39 mitigated vascular fibrosis, augmented endothelium-dependent vasodilation, and inhibited endothelial inflammation, oxidative stress, and apoptosis in mice. Additionally, GPR39 KO decreased NOD-like receptor protein 3 (Nlrp3) gene expression in Ang II-stimulated endothelial cells. Notably, Nlrp3 activa","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-06-03T05:15:27.113Z","creation":"2025-04-06T10:13:41.1Z"},"accession":"S-EPMC11538459","cross_references":{"pubmed":["39500998"],"doi":["10.1038/s42003-024-07132-2"]}}