{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(11)"],"submitter":["Renga B"],"pubmed_abstract":["<h4>Background</h4>GPBAR1 is a bile acids activated receptor expressed in entero-hepatic tissues. In the liver expression of GPBAR1 is restricted to sinusoidal and Kuppfer cells. In the systemic circulation vasodilation caused by GPBAR1 agonists is abrogated by inhibition of cystathione-γ-liase (CSE), an enzyme essential to the generation of hydrogen sulfide (H2S), a vasodilatory agent. Portal BAR501 is a semisynthetic bile acid derivative endowed with a potent and selective agonistic activity toward GPBAR1.<h4>Methods</h4>Cirrhosis was induced in mice by carbon tetrachloride (CCL4) administration for 9 weeks. Liver endothelial dysfunction was induced by feeding wild type and Gpbar1-/- mice with methionine for 4 weeks. In both models, mice were administered BAR501, 15 mg/kg/day.<h4>Results"],"journal":["PloS one"],"pagination":["e0141082"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4634759"],"repository":["biostudies-literature"],"pubmed_title":["Reversal of Endothelial Dysfunction by GPBAR1 Agonism in Portal Hypertension Involves a AKT/FOXOA1 Dependent Regulation of H2S Generation and Endothelin-1."],"pmcid":["PMC4634759"],"pubmed_authors":["Zampella A","Renga B","Cipriani S","Carino A","Fiorucci S","Simonetti M"],"additional_accession":[]},"is_claimable":false,"name":"Reversal of Endothelial Dysfunction by GPBAR1 Agonism in Portal Hypertension Involves a AKT/FOXOA1 Dependent Regulation of H2S Generation and Endothelin-1.","description":"<h4>Background</h4>GPBAR1 is a bile acids activated receptor expressed in entero-hepatic tissues. In the liver expression of GPBAR1 is restricted to sinusoidal and Kuppfer cells. In the systemic circulation vasodilation caused by GPBAR1 agonists is abrogated by inhibition of cystathione-γ-liase (CSE), an enzyme essential to the generation of hydrogen sulfide (H2S), a vasodilatory agent. Portal BAR501 is a semisynthetic bile acid derivative endowed with a potent and selective agonistic activity toward GPBAR1.<h4>Methods</h4>Cirrhosis was induced in mice by carbon tetrachloride (CCL4) administration for 9 weeks. Liver endothelial dysfunction was induced by feeding wild type and Gpbar1-/- mice with methionine for 4 weeks. In both models, mice were administered BAR501, 15 mg/kg/day.<h4>Results","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015","modification":"2025-06-01T12:02:47.526Z","creation":"2025-06-01T12:02:47.526Z"},"accession":"S-EPMC4634759","cross_references":{"pubmed":["26539823"],"doi":["10.1371/journal.pone.0141082"]}}