{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen JZ"],"funding":["NCATS NIH HHS","NHLBI NIH HHS"],"pagination":["2538-2550"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8458261"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(10)"],"pubmed_abstract":["Objective: A cardinal feature of Marfan syndrome is thoracic aortic aneurysm. The contribution of the renin-angiotensin system via AT1aR (Ang II [angiotensin II] receptor type 1a) to thoracic aortic aneurysm progression remains controversial because the beneficial effects of angiotensin receptor blockers have been ascribed to off-target effects. This study used genetic and pharmacological modes of attenuating angiotensin receptor and ligand, respectively, to determine their roles on thoracic aortic aneurysm in mice with fibrillin-1 haploinsufficiency (Fbn1C1041G/+)."],"journal":["Arteriosclerosis, thrombosis, and vascular biology"],"pubmed_title":["Deletion of AT1a (Angiotensin II Type 1a) Receptor or Inhibition of Angiotensinogen Synthesis Attenuates Thoracic Aortopathies in Fibrillin1<sup>C1041G/+</sup> Mice."],"pmcid":["PMC8458261"],"funding_grant_id":["UL1 TR001998","K01 HL149984","F30 HL143943","R01 HL133723"],"pubmed_authors":["Sheppard MB","Moorleghen JJ","Lu HS","Sawada H","Howatt DA","Kukida M","Ohno-Urabe S","Franklin MK","Mullick AE","Chen JZ","Ye D","Daugherty A","Katsumata Y"],"additional_accession":[]},"is_claimable":false,"name":"Deletion of AT1a (Angiotensin II Type 1a) Receptor or Inhibition of Angiotensinogen Synthesis Attenuates Thoracic Aortopathies in Fibrillin1<sup>C1041G/+</sup> Mice.","description":"Objective: A cardinal feature of Marfan syndrome is thoracic aortic aneurysm. The contribution of the renin-angiotensin system via AT1aR (Ang II [angiotensin II] receptor type 1a) to thoracic aortic aneurysm progression remains controversial because the beneficial effects of angiotensin receptor blockers have been ascribed to off-target effects. This study used genetic and pharmacological modes of attenuating angiotensin receptor and ligand, respectively, to determine their roles on thoracic aortic aneurysm in mice with fibrillin-1 haploinsufficiency (Fbn1C1041G/+).","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2026-03-31T10:53:02.414Z","creation":"2025-02-19T01:22:10.363Z"},"accession":"S-EPMC8458261","cross_references":{"pubmed":["34407634"],"doi":["10.1161/ATVBAHA.121.315715","10.1161/atvbaha.121.315715"]}}