Deletion of ACTA2 in mice promotes angiotensin II induced pathogenesis of thoracic aortic aneurysms and dissections | Zendy

Jiancheng Cheng | Zendy; Xianwu Zhou | Zendy; Xionggang Jiang | Zendy; Tucheng Sun | Zendy

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Deletion of ACTA2 in mice promotes angiotensin II induced pathogenesis of thoracic aortic aneurysms and dissections

Author(s) -

Jiancheng Cheng,

Xianwu Zhou,

Xionggang Jiang,

Tucheng Sun

Publication year - 2018

Publication title -

journal of thoracic disease

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.682

H-Index - 60

eISSN - 2077-6624

pISSN - 2072-1439

DOI - 10.21037/jtd.2018.07.75

Subject(s) - medicine , angiotensin ii , vascular smooth muscle , apoptosis , tunel assay , western blot , pathogenesis , aortic aneurysm , osteopontin , lumen (anatomy) , pathology , aorta , endocrinology , gene , immunohistochemistry , biology , smooth muscle , blood pressure , biochemistry

Mutation of the ACTA2 (α-2 smooth muscle actin) gene accounts for ~15% of all cases of familial thoracic aortic aneurysms and dissections. Surprisingly, no severe vascular phenotypes were observed at baseline in mice carrying this gene mutation. Our aim was to explore whether mutation of ACTA2 promotes the development of aneurysms or dissections in the presence of angiotensin II (AngII) and to determine whether this mutation has an impact on the phenotypic modulation and apoptosis mediated by AngII in vascular smooth muscle cells (VSMCs).

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