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Genetic basis of thoracic aortic aneurysms and dissections: focus on smooth muscle cell contractile dysfunction

Annual review of genomics and human genetics, 2008-01, Vol.9 (1), p.283-302

2008

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Pathogenesis of Thoracic and Abdominal Aortic Aneurysms

Annals of the New York Academy of Sciences, 2006-11, Vol.1085 (1), p.339-352

2006

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Fibulin-4 and fibulin-5 in elastogenesis and beyond: Insights from mouse and human studies

Matrix biology, 2014-07, Vol.37, p.142-149

2014

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Abnormal mechanosensing and cofilin activation promote the progression of ascending aortic aneurysms in mice

Science signaling, 2015-10, Vol.8 (399), p.ra105

2015

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Angiotensin-converting enzyme-induced activation of local angiotensin signaling is required for ascending aortic aneurysms in fibulin-4-deficient mice

Science translational medicine, 2013-05, Vol.5 (183), p.183ra58, 1

2013

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Characterization of the inflammatory cells in ascending thoracic aortic aneurysms in patients with Marfan syndrome, familial thoracic aortic aneurysms, and sporadic aneurysms

The Journal of thoracic and cardiovascular surgery, 2008-10, Vol.136 (4), p.922-929.e1

2008

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MMP17/MT4-MMP and Thoracic Aortic Aneurysms: OPNing New Potential for Effective Treatment

Circulation research, 2015-07, Vol.117 (2), p.109-112

2015

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Mutations in smooth muscle α-actin ( ACTA2 ) lead to thoracic aortic aneurysms and dissections

Nature genetics, 2007-12, Vol.39 (12), p.1488-1493

2007

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Loss of fibulin-4 disrupts collagen synthesis and maturation: implications for pathology resulting from EFEMP2 mutations

Human molecular genetics, 2015-10, Vol.24 (20), p.5867-5879

2015

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Loss of Smooth Muscle α-Actin Leads to NF-κB–Dependent Increased Sensitivity to Angiotensin II in Smooth Muscle Cells and Aortic Enlargement

Circulation research, 2017-06, Vol.120 (12), p.1903-1915

2017

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MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor 1 and angiotensin II

Human molecular genetics, 2007-10, Vol.16 (20), p.2453-2462

2007

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Smooth muscle hyperplasia due to loss of smooth muscle α-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-β

Human molecular genetics, 2013-08, Vol.22 (15), p.3123-3137

2013

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Genetic variants promoting smooth muscle cell proliferation can result in diffuse and diverse vascular diseases: Evidence for a hyperplastic vasculomyopathy

Genetics in medicine, 2010-04, Vol.12 (4), p.196-203

2010

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MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor1 and angiotensin II

Human molecular genetics, 2008-01, Vol.17 (1), p.158-158

2008

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Abstract 18657: Fibulin-4 Deficiency Alters Collagen Regulation in the Aortic Wall

Circulation (New York, N.Y.), 2013-11, Vol.128 (suppl_22)

2013

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Loss of Smooth Muscle α-actin Leads to NF-κB-Dependent Increased Sensitivity to Angiontensin II in Smooth Muscle Cells and Aortic Enlargement

Circulation research, 2017-05, Vol.120 (12), p.1903-1915

2017

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Abstract 458: Loss of Smooth Muscle α-actin in Mice Results in Thoracic Aortic Aneurysms via Increased Reactive Oxygen Species, Increased Nox4,and Increased Angiotensin II type 1 Receptor-Mediated Signaling

Arteriosclerosis, thrombosis, and vascular biology, 2015-05, Vol.35 (suppl_1)

2015

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Smooth muscle hyperplasia due to loss of smooth muscle [alpha]-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-[beta]

Human molecular genetics, 2013-08, Vol.22 (15), p.3123-3137

2013

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Abstract 2681: Mutations in Smooth Muscle-Specific Contractile Proteins Cause Familial Thoracic Aortic Aneurysms and Dissections and Lead to Increased IGF-1 Expression

Circulation (New York, N.Y.), 2007-10, Vol.116 (suppl_16)

2007

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Erratum: Corrigendum: Mutations in smooth muscle α-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Nature genetics, 2008-02, Vol.40 (2), p.255-255

2008

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Corrigendum: Mutations in smooth muscle [alpha]-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Nature genetics, 2008-02, Vol.40 (2), p.255

2008

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Corrigendum: Mutations in smooth muscle α-actin ( ACTA2 ) lead to thoracic aortic aneurysms and dissections

Nature genetics, 2008-02, Vol.40 (2), p.255-255

2008

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Correction: Corrigendum: Mutations in smooth muscle α-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Nature genetics, 2008, Vol.40 (2), p.255-255

2008

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Mutations in smooth muscle [alpha]-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Nature genetics, 2007-12, Vol.39 (12), p.1488-1493

2007

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Genetic basis of thoracic aortic aneurysms and dissections: focus on smooth muscle cell contractile dysfunction

Pathogenesis of Thoracic and Abdominal Aortic Aneurysms

Fibulin-4 and fibulin-5 in elastogenesis and beyond: Insights from mouse and human studies

Abnormal mechanosensing and cofilin activation promote the progression of ascending aortic aneurysms in mice

Angiotensin-converting enzyme-induced activation of local angiotensin signaling is required for ascending aortic aneurysms in fibulin-4-deficient mice

Characterization of the inflammatory cells in ascending thoracic aortic aneurysms in patients with Marfan syndrome, familial thoracic aortic aneurysms, and sporadic aneurysms

MMP17/MT4-MMP and Thoracic Aortic Aneurysms: OPNing New Potential for Effective Treatment

Mutations in smooth muscle α-actin ( ACTA2 ) lead to thoracic aortic aneurysms and dissections

Loss of fibulin-4 disrupts collagen synthesis and maturation: implications for pathology resulting from EFEMP2 mutations

Mutations in Smooth Muscle Alpha-Actin (ACTA2) Cause Coronary Artery Disease, Stroke, and Moyamoya Disease, Along with Thoracic Aortic Disease

Loss of Smooth Muscle α-Actin Leads to NF-κB–Dependent Increased Sensitivity to Angiotensin II in Smooth Muscle Cells and Aortic Enlargement

MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor 1 and angiotensin II

Smooth muscle hyperplasia due to loss of smooth muscle α-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-β

Genetic variants promoting smooth muscle cell proliferation can result in diffuse and diverse vascular diseases: Evidence for a hyperplastic vasculomyopathy

MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor1 and angiotensin II

Abstract 18657: Fibulin-4 Deficiency Alters Collagen Regulation in the Aortic Wall

Loss of Smooth Muscle α-actin Leads to NF-κB-Dependent Increased Sensitivity to Angiontensin II in Smooth Muscle Cells and Aortic Enlargement

Abstract 458: Loss of Smooth Muscle α-actin in Mice Results in Thoracic Aortic Aneurysms via Increased Reactive Oxygen Species, Increased Nox4,and Increased Angiotensin II type 1 Receptor-Mediated Signaling

Smooth muscle hyperplasia due to loss of smooth muscle [alpha]-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-[beta]

Abstract 2681: Mutations in Smooth Muscle-Specific Contractile Proteins Cause Familial Thoracic Aortic Aneurysms and Dissections and Lead to Increased IGF-1 Expression

Erratum: Corrigendum: Mutations in smooth muscle α-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Corrigendum: Mutations in smooth muscle [alpha]-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Corrigendum: Mutations in smooth muscle α-actin ( ACTA2 ) lead to thoracic aortic aneurysms and dissections

Correction: Corrigendum: Mutations in smooth muscle α-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

Mutations in smooth muscle [alpha]-actin (ACTA2) lead to thoracic aortic aneurysms and dissections

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