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

doi:10.1161/ATVBAHA.121.315715

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

Arteriosclerosis, thrombosis, and vascular biology - 1 Oct 2021

Chen Jeff Z, Sawada Hisashi, Ye Dien, Katsumata Yuriko, Kukida Masayoshi, Ohno-Urabe Satoko, Moorleghen Jessica J, Franklin Michael K, Howatt Deborah A, Sheppard Mary B, Mullick Adam E, Lu Hong S, Daugherty Alan

Abstract excerpt

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...

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

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