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Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

http://www.wikidata.org/entity/Q37602214

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Marfan syndrome: current perspectives Mechanotransduction and extracellular matrix homeostasis Heading in the Right Direction: Understanding Cellular Orientation Responses to Complex Biophysical Environments Adamtsl2 deletion results in bronchial fibrillin microfibril accumulation and bronchial epithelial dysplasia--a novel mouse model providing insights into geleophysic dysplasia Heart Failure in Pediatric Patients With Congenital Heart Disease.Fibrillin microfibrils in bone physiology.Left ventricular systolic dysfunction in asymptomatic Marfan syndrome patients is related to the severity of gene mutation: insights from the novel three dimensional speckle tracking echocardiography.Role of mechanotransduction in vascular biology: focus on thoracic aortic aneurysms and dissections.A Perspective on Studying G-Protein-Coupled Receptor Signaling with Resonance Energy Transfer Biosensors in Living Organisms.Losartan ameliorates dystrophic epidermolysis bullosa and uncovers new disease mechanisms Aortic and Cardiac Structure and Function Using High-Resolution Echocardiography and Optical Coherence Tomography in a Mouse Model of Marfan Syndrome.A Role for Photobiomodulation in the Prevention of Myocardial Ischemic Reperfusion Injury: A Systematic Review and Potential Molecular Mechanisms.The role of β-arrestin2-dependent signaling in thoracic aortic aneurysm formation in a murine model of Marfan syndrome.Fibrillin-containing microfibrils are key signal relay stations for cell function.Cardiac remodeling in the mouse model of Marfan syndrome develops into two distinctive phenotypes Problems in biology with many scales of length: Cell-cell adhesion and cell jamming in collective cellular migration.Smooth muscle cell-specific Tgfbr1 deficiency promotes aortic aneurysm formation by stimulating multiple signaling events.The effect of losartan therapy on ventricular function in Marfan patients with haploinsufficient or dominant negative FBN1 mutations ADAMTS-10 and -6 differentially regulate cell-cell junctions and focal adhesions.Ventricular-Vascular Coupling in Marfan and Non-Marfan Aortopathies Angiotensin receptor blockade mediated amelioration of mucopolysaccharidosis type I cardiac and craniofacial pathology.Nonmyocyte ERK1/2 signaling contributes to load-induced cardiomyopathy in Marfan mice.Therapeutics Targeting Drivers of Thoracic Aortic Aneurysms and Acute Aortic Dissections: Insights from Predisposing Genes and Mouse Models.Sex, pregnancy and aortic disease in Marfan syndrome.The N-Terminal Region of Fibrillin-1 Mediates a Bipartite Interaction with LTBP1.Abnormal mechanosensing and cofilin activation promote the progression of ascending aortic aneurysms in mice.Cardiovascular Benefits of Moderate Exercise Training in Marfan Syndrome: Insights From an Animal Model.Fell-Muir Lecture: Fibrillin microfibrils: structural tensometers of elastic tissues?Type B aortic dissection triggered by heart transplantation in a patient with Marfan syndrome.5th International Meeting on Aortic Diseases: New Insights into an Old Problem.Crossing Bridges between Extra- and Intra-Cellular Events in Thoracic Aortic Aneurysms.Cell Type-Specific Contributions of the Angiotensin II Type 1a Receptor to Aorta Homeostasis and Aneurysmal Disease.Marfan syndrome; A connective tissue disease at the crossroads of mechanotransduction, TGFβ signaling and cell stemness.Heart failure and sudden cardiac death in heritable thoracic aortic disease caused by pathogenic variants in the SMAD3 gene

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Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

http://www.wikidata.org/entity/Q37602214

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 17 February 2014

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

@en

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

@nl

type

label

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

@en

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

@nl

prefLabel

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

@en

Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.

@nl

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Journal of Clinical Investigation

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Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome

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Elie R Chemaly

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Emily Chiu

http://www.w3.org/2001/XMLSchema#string

Francesco Ramirez

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GenTAC Registry Consortium

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Jason R Cook

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Kevin D Costa

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Luca Carta

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Ludovic Bénard

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Roger J Hajjar

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Satish K Rao

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P2860

Evidence for a critical contribution of haploinsufficiency in the complex pathogenesis of Marfan syndrome

Conformational switch of angiotensin II type 1 receptor underlying mechanical stress-induced activation

Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome

Measurement of cardiac function using pressure-volume conductance catheter technique in mice and rats

Pathogenetic sequence for aneurysm revealed in mice underexpressing fibrillin-1

Dynamic correction for parallel conductance, GP, and gain factor, alpha, in invasive murine left ventricular volume measurements

Signaling effectors underlying pathologic growth and remodeling of the heart

The cell biology of disease: cellular mechanisms of cardiomyopathy.

The genetic basis for cardiomyopathy: from mutation identification to mechanistic paradigms

Angiotensin II blockade reverses myocardial fibrosis in a transgenic mouse model of human hypertrophic cardiomyopathy

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1329-1339

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10.1172/JCI71059

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