562 research outputs found
Bleeding rate during oral surgery of oral anticoagulant therapy patients with associated systemic pathologic entities: a prospective study of more than 500 extractions
Prediction of atrial fibrillation recurrence after cardioversion in patients with left-atrial dilation.
Noninvasive Assessment of Hemodynamic Status in HeartWare Left Ventricular Assist Device Patients. Validation of an Echocardiographic Approach
Transoesophageal echocardiography in patients without arterial and major cardiac sources of embolism: difference between stroke subtypes.
Left Atrial Function After Radiofrequency Catheter Ablation of Atrial Fibrillation--Can Pre-Ablation Function Predict Contractile Improvement During Follow-up?
Increased epicardial fat and early signs of impaired diastolic and systolic left ventricular function in non-diabetic, non-dyslipidemic, normotensive patients with Nonalcoholic Fatty Liver Disease
Insulin resistance and liver damage are associated with early signs of left ventricular systolic dysfunction in patients with Non Alcoholic Fatty Liver Disease independent of diabetes, hypertension and dyslipidemia
STAT3 activity is necessary and sufficient for the development of immune-mediated myocarditis in mice and promotes progression to dilated cardiomyopathy
Activated Met Signalling in the Developing Mouse Heart Leads to Cardiac Disease
BACKGROUND: The Hepatocyte Growth Factor (HGF) is a pleiotropic cytokine involved in many physiological processes, including skeletal muscle, placenta and liver development. Little is known about its role and that of Met tyrosine kinase receptor in cardiac development. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we generated two transgenic mice with cardiac-specific, tetracycline-suppressible expression of either Hepatocyte Growth Factor (HGF) or the constitutively activated Tpr-Met kinase to explore: i) the effect of stimulation of the endogenous Met receptor by autocrine production of HGF and ii) the consequence of sustained activation of Met signalling in the heart. We first showed that Met is present in the neonatal cardiomyocytes and is responsive to exogenous HGF. Exogenous HGF starting from prenatal stage enhanced cardiac proliferation and reduced sarcomeric proteins and Connexin43 (Cx43) in newborn mice. As adults, these transgenics developed systolic contractile dysfunction. Conversely, prenatal Tpr-Met expression was lethal after birth. Inducing Tpr-Met expression during postnatal life caused early-onset heart failure, characterized by decreased Cx43, upregulation of fetal genes and hypertrophy. CONCLUSIONS/SIGNIFICANCE: Taken together, our data show that excessive activation of the HGF/Met system in development may result in cardiac damage and suggest that Met signalling may be implicated in the pathogenesis of cardiac disease
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