Aggressive cardiovascular phenotype of aneurysms-osteoarthritis syndrome caused by pathogenic SMAD3 variants.

[1]  J. Roos‐Hesselink,et al.  Saccular aneurysm within a persistent ductus arteriosus , 2012, The Lancet.

[2]  G. Pals,et al.  Phenotypic spectrum of the SMAD3-related aneurysms–osteoarthritis syndrome , 2011, Journal of Medical Genetics.

[3]  Mike Kirby,et al.  Guidelines on the management of cardiovascular diseases during pregnancy The Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology ( ESC ) , 2011 .

[4]  M. Rieder,et al.  Exome Sequencing Identifies SMAD3 Mutations as a Cause of Familial Thoracic Aortic Aneurysm and Dissection With Intracranial and Other Arterial Aneurysms , 2011, Circulation research.

[5]  S. Bamforth,et al.  TGFβ signaling and congenital heart disease: Insights from mouse studies. , 2011, Birth defects research. Part A, Clinical and molecular teratology.

[6]  Jeroen J. Bax,et al.  Usefulness of repeated N-terminal pro-B-type natriuretic peptide measurements as incremental predictor for long-term cardiovascular outcome after vascular surgery. , 2011, The American journal of cardiology.

[7]  G. Vriend,et al.  Mutations in SMAD3 cause a syndromic form of aortic aneurysms and dissections with early-onset osteoarthritis , 2011, Nature Genetics.

[8]  J. Camm,et al.  Assessment of Aortic Stiffness in Marfan Syndrome Using Two‐Dimensional and Doppler Echocardiography , 2011, Echocardiography.

[9]  Roger R Markwald,et al.  Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β. , 2010, The Journal of clinical investigation.

[10]  Joyce Wong,et al.  Evidence for Marfan cardiomyopathy , 2010, European journal of heart failure.

[11]  T. Munzel,et al.  Atrial fibrosis and atrial fibrillation: the role of the TGF-β1 signaling pathway. , 2010, International journal of cardiology.

[12]  Yasmin,et al.  Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: ‘establishing normal and reference values’ , 2010, European heart journal.

[13]  P. Robinson,et al.  Augmentation index and the evolution of aortic disease in marfan-like syndromes. , 2010, American Journal of Hypertension.

[14]  David M. Williams,et al.  2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, Ame , 2010, Journal of the American College of Cardiology.

[15]  Fengjuan Yao,et al.  B‐type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor‐β1/smad7 pathway in vivo and in vitro , 2010, Clinical and Experimental Pharmacology and Physiology.

[16]  J. Floras,et al.  Endothelial function, carotid-femoral stiffness, and plasma matrix metalloproteinase-2 in men with bicuspid aortic valve and dilated aorta. , 2010, Journal of the American College of Cardiology.

[17]  David M. Williams,et al.  2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Th , 2010, Anesthesia and analgesia.

[18]  D. Yousem,et al.  Neuroradiologic Manifestations of Loeys-Dietz Syndrome Type 1 , 2009, American Journal of Neuroradiology.

[19]  T. Tadros,et al.  Ascending aortic dilatation associated with bicuspid aortic valve: pathophysiology, molecular biology, and clinical implications. , 2009, Circulation.

[20]  P. Byers,et al.  Aneurysm syndromes caused by mutations in the TGF-beta receptor. , 2006, The New England journal of medicine.

[21]  George H. Thomas,et al.  Aneurysm Syndromes Caused by Mutations in the TGF-β Receptor , 2006 .

[22]  M. Maganti,et al.  Long-term results of aortic valve-sparing operations for aortic root aneurysm. , 2006, Journal of Thoracic and Cardiovascular Surgery.

[23]  R. Sheppard,et al.  Fibrosis in heart disease: understanding the role of transforming growth factor‐β1 in cardiomyopathy, valvular disease and arrhythmia , 2006, Immunology.

[24]  Wolfram Kress,et al.  A syndrome of altered cardiovascular, craniofacial, neurocognitive and skeletal development caused by mutations in TGFBR1 or TGFBR2 , 2005, Nature Genetics.

[25]  Joyce Bischoff,et al.  Heart valve development: endothelial cell signaling and differentiation. , 2004, Circulation research.

[26]  S. Rosenkranz.  TGF-β1 and angiotensin networking in cardiac remodeling , 2004 .

[27]  K. Nath,et al.  Marfan's syndrome. , 1959, Journal of the Indian Medical Association.

[28]  Jeroen J. Bax,et al.  Natriuretic peptide levels predict recurrence of atrial fibrillation after radiofrequency catheter ablation. , 2011, American Heart Journal.

[29]  J. Stockman,et al.  Angiotensin II Blockade and Aortic-Root Dilation in Marfan's Syndrome , 2010 .

[30]  S. Rosenkranz.  TGF-beta1 and angiotensin networking in cardiac remodeling. , 2004, Cardiovascular research.