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http://dx.doi.org/10.1161/CIRCRESAHA.117.306851 | DOI Listing |
Circ Res
July 2015
From the Department of Molecular Biology, UT Southwestern Medical Center, Dallas, TX (C.L.P., H.Y.); and Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Ibaraki, Japan (Y.Y., H.Y.).
Circ Res
July 2015
From the Department of Vascular Biology and Inflammation (M.M.-A., A.A., N.M.-B., A.P., J.M.R., A.G.A.), Proteomics Unit (E.C., J.V.) and Bioinformatics Unit (F.M.), Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; Department of Pharmacology/Nephrology, Faculty of Medicine, Universidad Autónoma de Madrid, Madrid, Spain (A.B.G.-R., M.S.); Department of Internal Medicine, University of Texas Health Science Center at Houston, TX (D.G., D.M.); Department of Basic Biomedical Sciences, Universidad Europea de Madrid, Villaviciosa de Odón, Madrid, Spain (C.S.-C.); Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ (D.T.D.); and Division of Cancer Cell Research, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan (M.S.).
Rationale: Aortic dissection or rupture resulting from aneurysm causes 1% to 2% of deaths in developed countries. These disorders are associated with mutations in genes that affect vascular smooth muscle cell differentiation and contractility or extracellular matrix composition and assembly. However, as many as 75% of patients with a family history of aortic aneurysms do not have an identified genetic syndrome.
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