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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).

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