REsearch

 

Embryonic hearts establish a synchronized and rhythmic contraction pattern to circulate blood through the body. We have shown that the zebrafish tremblor (tre) locus encodes a cardiac-specific sodium calcium exchanger gene (NCX1h). Embryos deficient in NCX1h have abnormal calcium transients and develop a fibrillating heart, indicating a critical role of calcium homeostasis in maintaining embryonic cardiac rhythmicity.

From a collection of novel small molecules, we identified a chemical suppressor of cardiac fibrillation. Applying this compound on the fibrillating tre mutant heart can suppress the chaotic contraction of cardiomyocytes and restore synchronized contraction patterns. We have identified the protein target of this compound by biochemical and molecular approaches.  We are currently studying mechanisms by which compound and its target protein control calcium handling and cardiac rhythmicity at the molecular and physiological levels.

Cardiac Rhythmicity