Abstract
This review focuses on the role and the molecular candidates of the cardiac stretch-activated potassium current (SAK). The functional properties of the two-pore domain potassium (K2P) channel TREK-1, a major candidate for the cardiac SAK, are analyzed and the molecular mechanism of stretch-activation in K2P potassium channels is discussed. Furthermore, the functional modulation of TREK-1 by different cardiac interaction partners, as well as evidence for the functional role of the stretch-dependent TREK-1 and its putative subunits in the heart is reviewed. In addition, we summarize the recent evidence that TREK-1 is involved in the pathogenesis of human cardiac arrhythmias.
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