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Deletion of AT1a (Angiotensin II Type 1a) Receptor or Inhibition of Angiotensinogen Synthesis Attenuates Thoracic Aortopathies in Fibrillin1C1041G/+ Mice.

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/+).

SUBMITTER: Chen JZ 

PROVIDER: S-EPMC8458261 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature

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Deletion of AT1a (Angiotensin II Type 1a) Receptor or Inhibition of Angiotensinogen Synthesis Attenuates Thoracic Aortopathies in Fibrillin1<sup>C1041G/+</sup> Mice.

Chen Jeff Z JZ   Sawada Hisashi H   Ye Dien D   Katsumata Yuriko Y   Kukida Masayoshi M   Ohno-Urabe Satoko S   Moorleghen Jessica J JJ   Franklin Michael K MK   Howatt Deborah A DA   Sheppard Mary B MB   Sheppard Mary B MB   Mullick Adam E AE   Lu Hong S HS   Daugherty Alan A  

Arteriosclerosis, thrombosis, and vascular biology 20210819 10

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 aor  ...[more]

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