TRPC3 contributes to regulation of cardiac contractility and arrhythmogenesis by dynamic interaction with NCX1

Conclusion
Cardiac TRPC3 mediates Ca2+ and Na+ entry in proximity of NCX1, thereby elevating cellular Ca2+ levels and contractility. Excessive activation of TRPC3 is associated with transient cellular Ca2+ overload, spatial uncoupling between TRPC3 and NCX1, and arrhythmogenesis. We propose TRPC3-NCX micro/nanodomain communication as determinant of cardiac contractility and susceptibility to arrhythmogenic stimuli.

Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Doleschal, B., Primessnig, U., Wolkart, G., Wolf, S., Schernthaner, M., Lichtenegger, M., Glasnov, T. N., Kappe, C. O., Mayer, B., Antoons, G., Heinzel, F., Poteser, M., Groschner, K. Tags: Ion channels and arrhythmias Source Type: research