Project description:We investigated genetic background of familial and early onset atrial fibrillation (AF) with the aim of identify genes involved in atrial fibrillation pathology and are highly predisposing risk factors. We performed whole exome sequencing on 24 families where three or more family members suffered from AF.
Project description:Atrial fibrillation (AF) is the most common heart arrhythmia disease. The greatest risk of atrial fibrillation is stroke, and stroke caused by valvular heart disease with atrial fibrillation (AF-VHD) is more serious. the development mechanism from VHD to AF-VHD is not yet clear. The research on expression profiles of lncRNA and mRNA is helpful to explore molecular mechanism in patients with valvular heart disease who develop atrial fibrillation.
Project description:Atrial fibrillation (AF) is the most common persistent arrhythmia that affect 1–2% of the general population. People with AF display an array of complications cardiogenic stroke and systemic embolism caused by hemodynamic instability and blood hypercoagulability in clinical practice. However, it’s still unclear whether and how ubiquitylated proteins react to AF in the left atrial appendage of patients with AF and valvular heart disease. This theory focuses on the changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease. We firstly widely analysis the proteins ubiquitination in patients with atrial fibrillation.
Project description:Atrial fibrillation is associated with stuctural remodelling of the atria that involves various cell types, including cardiac myocytes, endothelial cells, and immune cells. Atrial myopathy forms the substrate for an increased risk for AF onset and on the other hand AF drives atrial myopathy. Atrial myopathy is linked to risk factors such as aging, hypertension, obesity, or heart failure. Aldosterone and the mineralocorticoid receptor are drivers of pathological remodeling in atrial myopathy. In this study, we investigated the effect of aldosterone on left atrial gene expression and cell-cell communication.
Project description:<p>The Massachusetts General Hospital (MGH) Atrial Fibrillation Study was initiated in 2001. The study has enrolled serial probands, unaffected and affected family members with atrial fibrillation. At enrollment participants undergo a structured interview to systematically capture their past medical history, AF treatments, and family history. An electrocardiogram is performed; the results of an echocardiogram are obtained; and blood samples are obtained.</p> <p>For the TOPMed WGS project only early-onset atrial fibrillation cases were sequenced. Early-onset atrial fibrillation was defined as an age of onset prior to 66 years of age.</p> <p>Comprehensive phenotypic and pedigree data for study participants are available through dbGaP <a href="./study.cgi?study_id=phs001001">phs001001</a>.</p>
Project description:Cardiac fibrosis is the key to the onset of atrial fibrillation (AF), but the mechanism is not fully understood. Our previous study found that fibrosis-related adipocytokines were dysregulated in epicardial adipose tissue (EAT) from patients with AF. In this study, we explored the factor that induce adipocytokines dysregulation and the mechanism underlying adipocytokines dysregulation-induced cardiac fibrosis.
Project description:<p>The Massachusetts General Hospital (MGH) Atrial Fibrillation Study was initiated in 2001. The study has enrolled serial probands, unaffected and affected family members with atrial fibrillation. At enrollment participants undergo a structured interview to systematically capture their past medical history, AF treatments, and family history. An electrocardiogram is performed; the results of an echocardiogram are obtained; and blood samples are obtained.</p> <p><b>The Massachusetts General Hospital (MGH) Atrial Fibrillation Study is utilized in the following dbGaP substudies.</b> To view genotypes, analysis, other molecular data, and derived variables collected in these substudies, please click on the following substudies below or in the "Substudies" box located on the right hand side of this top-level study page phs001001 Massachusetts General Hospital (MGH) Atrial Fibrillation Study. <ul> <li><a href="./study.cgi?study_id=phs001116">phs001116</a> MGH AF CHARGE-S</li> <li><a href="./study.cgi?study_id=phs001117">phs001117</a> MGH AF Exome Sequencing</li> <li><a href="./study.cgi?study_id=phs001118">phs001118</a> MGH AF Medical Resequencing</li> </ul> </p>
Project description:Atrial fibrillation (AF) is currently the most prevalent arrhythmia worldwide.Recent clinical data implicate the additional contribution of non-coding RNAs in the pathogenesis of AFï¼which include microRNAs(miRNAs), endogenous small interfering RNAs, PIWIinteracting RNAs, and lncRNA. Notably, a growing number of lncRNAs have been implicated in disease etiology, although an association with AF has not been reported. In the present study, we conducted an integrated analysis of dysregulated lncRNA and mRNA expression profiles in myocardial sleevesof pulmonary veins between the patients who develop AF and the patients who were in normal sinus rhythm, which was performed using a second generation lncRNA microarrayï¼focusing specifically on the identification and characterization of lncRNAs and mRNA potentially involving in maintaining atrial fibrillation. We conducted an integrated analysis of myocardial sleeves of pulmonary veinsï¼PVsï¼from 12 patients (6 non-AF and 6AF) in our center, of which hypertension, diabetes, smoking and alcohol abuse were excluded, using a second generation lncRNA microarray