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Reversal of cardiomyocyte remodeling in Atrial Fibrillation; the role of protein degradation and translation modulators

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Title:  Reversal of cardiomyocyte remodeling in Atrial Fibrillation; the role of protein degradation and translation modulators
Investigator:   M Wiersma
Promoter: RH Henning
Co-promoter:  BJJM Brundel
 Summary: Atrial Fibrillation (AF) is the most common cardiac arrhythmia and strongly related to ageing. Unfortunately, treatment of AF is difficult, which is rooted in the persistent nature of the disease. AF persistence is caused by progressive changes in cardiomyocytes (‘remodeling’), increasing the vulnerability for the arrhythmia: ‘AF begets AF’. As the structural damage to cardiomyocytes is irreversible, it obstructs restoration of normal rhythm after pharmacological and electrical cardioversion. Importantly, most AF patients already experience structural damage at the moment of diagnosis. We investigate if the reversal of structural damage represents a key target to accomplish and maintain normal cardiac sinus rhythm after AF conversion. It is the aim of this project to uncover mechanisms that enhance structural restoration and revive cardiomyocyte function in AF.

The specific aims are to 1) examine the effect of modulation of protein degradation (autophagy/mitophagy) on the reversibility of structural remodeling, and 2) study the effect of autophagy/mitophagy modulating compounds on the reversibility of remodeling.

Financing: GSMS, PhD student
 
Start: 01-01-2013
End: 01-01-2016

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Reversal of cardiomyocyte remodeling in Atrial Fibrillation; the role of protein degradation and translation modulators.
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