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Calcium Propagation in Atrial Fibrillation

Calcium Propagation in Atrial Fibrillation

Objective

Synchronized release of Ca2+ from the internal Ca2+ store of cardiac myocytes, the sarcoplasmic reticulum, is essential for a normal heart beat. This is obtained through a sophisticated subcellular organization, the dyad. In dyads, a cluster of release channels in the sarcoplasmic reticulum, ryanodine receptors or RyRs, face Ca2+ channels in the cell membrane, the dihydropyrydine receptors or DHPRs. DHPRs provide the Ca2+ influx that triggers opening of RyR. Ca2+ release can also propagate between RyR, leading to Ca2+ waves that can initiate arrhythmias. We hypothesize that RyR that are not within dyads have different properties that may facilitate wave-like propagation and arrhythmias. The objectives are (1) to identify and characterize RyR located between dyads in the sarcomeric space in healthy myocytes (2) to establish whether altered organization and properties of RyRs in chronic atrial fibrillation (AF) contribute to the contractile dysfunction and arrhythmia in AF. My stay in the host lab will provide a clinical and translational perspective to my current knowledge enhancing the potential impact of my research. An interdisciplinary approach for imaging of RyR with access to novel microscopic techniques in the Molecular engineering department and tools for image analysis with the Medical Imaging Center and ESAT will enhance my technological expertise.
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Coordinator

KATHOLIEKE UNIVERSITEIT LEUVEN

Address

Oude Markt 13
3000 Leuven

Belgium

Activity type

Higher or Secondary Education Establishments

EU Contribution

€ 166 800

Administrative Contact

Delauré Stijn (Dr.)

Project information

Grant agreement ID: 255264

Status

Closed project

  • Start date

    1 March 2010

  • End date

    29 February 2012

Funded under:

FP7-PEOPLE

  • Overall budget:

    € 166 800

  • EU contribution

    € 166 800

Coordinated by:

KATHOLIEKE UNIVERSITEIT LEUVEN

Belgium