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Project

Ryanodine receptor heterogeneity in cardiac myocytes in ischemic cardiomyopathy after myocardial infarction

Ventricular arrhythmias can be an unwanted consequence after myocardial infarction and are a major cause of mortality worldwide. A large fraction of these arrhythmias are thought to be initiated and perpetuated through a loss of a normal intracellular calcium balance, causing abnormal electrical activity and proarrhythmogenic events. In the current project, we will examine the changes in one of the key proteins that regulate the calcium balance in the heart muscle cells, the ryanodine receptor. We will use imaging tools to dissect different ryanodine receptor subpopulations and investigate how modulation after myocardial infarction may affect the regulation of different RyR subsets. The impact on local changes will be investigated in different regions of the heart and translated to the whole heart. In parallel these findings will be validated in human cardiac myocytes and these results will provide novel insights into the underlying mechanisms causing arrhythmias and may thereby contribute to the development of a specific targeted therapy after ischemic heart disease.

Date:1 Oct 2016 →  31 Oct 2019
Keywords:Ryanodine receptor heterogeneity, ischemic cardiomyopathy, myocardial infarction, cardiac myocytes
Disciplines:Cardiac and vascular medicine