与慢性肾脏病相关的心房颤动的机制-猫眼课题宝

与慢性肾脏病相关的心房颤动的机制

批准号：

9913385

负责人：

Na Li

金额：

$51.06万

依托单位：

BAYLOR COLLEGE OF MEDICINE

依托单位国家：

美国

项目类别：

财政年份：

2019

资助国家：

美国

项目状态：

已结题

起止时间：

2019-04-15 至 2023-02-28

来源：

https://reporter.nih.gov/project-details/9913385

关键词：

Adult Affect American Arrhythmia Atrial Fibrillation CASP1 gene Calcium Cardiac Cardiac Myocytes Cardiovascular system Chronic Kidney Failure Confocal Microscopy Data Dependovirus Development Diagnosis Dietary Proteins Electric Stimulation Electrocardiogram Event Exhibits Goals Heart Atrium Hemorrhage Incidence Inflammasome Inflammation Ischemic Stroke Knock-in Mouse Knockout Mice Measures Mediating Molecular Monitor Morbidity - disease rate Mus Muscle Cells Nephrectomy Pathogenesis Pathway interactions Patients Pharmacology Phosphorylation Phosphorylation Site Play Predisposition Prevalence Prevention strategy Proteins Public Health Risk Risk Factors Rodent Model Role Ryanodine Receptor Calcium Release Channel Sinus Site Source Sterility Striated Muscles Telemetry Testing Tissues Work cardiovascular risk factor cohort dietary manipulation genetic regulatory protein knock-down mortality mouse model novel patch clamp prevent receptor receptor expression targeted treatment treatment strategy

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PROJECT SUMMARY / ABSTRACT Chronic kidney disease (CKD) is a known predictor of cardiovascular morbidity and mortality, and is an important risk factor for atrial fibrillation (AF). Very little remains known about the molecular mechanisms underlying AF associated with CKD. Our preliminary data reveal activation of the NLRP3 inflammasome within atrial myocytes isolated in a mouse model of CKD. The long-term goal of this project is to elucidate the molecular and cellular mechanisms underlying AF development as a result of inflammasome activation in mice with CKD. We will test the hypothesis that enhanced activation of the NLRP3 inflammasome within atrial myocytes enhances the susceptibility to AF by promoting proarrhythmogenic Ca2+ releases via increased SPEG-phosphorylation of RyR2.

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