{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Teixeira LB"],"funding":["CIHR"],"pubmed_abstract":["The renin-angiotensin system (RAS) plays a key role in the control of vasoconstriction as well as sodium and fluid retention mediated mainly by angiotensin (Ang) II acting at the AT<sub>1</sub> receptor (AT1R). Ang-(1-7) is another RAS peptide, identified as the endogenous ligand of the Mas receptor and known to counterbalance many of the deleterious effects of AngII. AT1R signaling triggered by β-arrestin-biased agonists has been associated to cardioprotection. Because position 8 in AngII is important for G protein activation, we hypothesized that Ang-(1-7) could be an endogenous β-arrestin-biased agonist of the AT1R. Here we show that Ang-(1-7) binds to the AT1R without activating Gq, but triggering β-arrestins 1 and 2 recruitment and activation. Using an in vivo model of cardiac hypertr"],"journal":["Scientific reports"],"pagination":["11903"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5605686"],"repository":["biostudies-literature"],"pubmed_title":["Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT<sub>1</sub> receptor with protective action in cardiac hypertrophy."],"pmcid":["PMC5605686"],"pubmed_authors":["Oliveira EB","Parreiras-E-Silva LT","Duarte DA","Bouvier M","Costa RM","Simoes SC","Silva CAA","Ferreira PAB","Abrao EP","Rodriguez DY","Costa-Neto CM","Teixeira LB","Bruder-Nascimento T","Tostes RC"],"additional_accession":[]},"is_claimable":false,"name":"Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT<sub>1</sub> receptor with protective action in cardiac hypertrophy.","description":"The renin-angiotensin system (RAS) plays a key role in the control of vasoconstriction as well as sodium and fluid retention mediated mainly by angiotensin (Ang) II acting at the AT<sub>1</sub> receptor (AT1R). Ang-(1-7) is another RAS peptide, identified as the endogenous ligand of the Mas receptor and known to counterbalance many of the deleterious effects of AngII. AT1R signaling triggered by β-arrestin-biased agonists has been associated to cardioprotection. Because position 8 in AngII is important for G protein activation, we hypothesized that Ang-(1-7) could be an endogenous β-arrestin-biased agonist of the AT1R. Here we show that Ang-(1-7) binds to the AT1R without activating Gq, but triggering β-arrestins 1 and 2 recruitment and activation. Using an in vivo model of cardiac hypertr","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Sep","modification":"2025-04-19T03:33:04.338Z","creation":"2019-03-27T02:56:52Z"},"accession":"S-EPMC5605686","cross_references":{"pubmed":["28928410"],"doi":["10.1038/s41598-017-12074-3"]}}