Mechanisms underlying atrial fibrillation associated with chronic kidney disease
Mechanisms underlying atrial fibrillation associated with chronic kidney disease
批准号:
10376782
负责人:
Na Li
金额:
$51.06万
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 2024-02-29
关键词:
AdultAffectAmericanArrhythmiaAtrial FibrillationCASP1 geneCalciumCardiacCardiac MyocytesCardiovascular systemChronic Kidney FailureConfocal MicroscopyDataDependovirusDevelopmentDiagnosisDietary ProteinsElectric StimulationElectrocardiogramEventExhibitsGoalsHeart AtriumHemorrhageIncidenceInflammasomeInflammationIschemic StrokeKnock-in MouseKnockout MiceMeasuresMediatingMolecularMonitorMorbidity - disease rateMusMuscle CellsNephrectomyPathogenesisPathway interactionsPatientsPharmacologyPhosphorylationPhosphorylation SitePlayPredispositionPrevalencePrevention strategyProteinsPublic HealthRiskRisk FactorsRodent ModelRoleRyanodine Receptor Calcium Release ChannelSinusSiteSourceSterilityStriated MusclesTelemetryTestingTissuesWorkantagonistcardiovascular risk factorcohortdietary manipulationgenetic regulatory proteinknock-downmortalitymouse modelnovelpatch clamppreventreceptorreceptor expressiontargeted treatmenttreatment strategy
中文摘要
项目摘要/摘要
慢性肾脏疾病(CKD)是心血管疾病发病率和死亡率的已知预测因子,是一种
房颤的重要危险因素。目前对其分子机制知之甚少。
与CKD相关的潜在房颤。我们的初步数据显示NLRP3炎症体在
慢性肾脏病小鼠模型中分离的心房肌细胞。这个项目的长期目标是阐明
炎性小体激活致小鼠房颤发生的分子和细胞机制
与CKD合作。我们将验证这样一种假设,即心房内NLRP3炎症小体的激活增强
心肌细胞通过增加钙离子释放促进诱发心律失常的钙离子释放,增强房颤的易感性
SpeG-RyR2的磷酸化。
英文摘要
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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