Sodium leak through K2P potassium channels and cardiac arrhythmia, an emerging theme.
- Author(s): Goldstein, Steve An
- et al.
Published Web Locationhttps://doi.org/10.15252/emmm.201607479
© 2017 EMBO. In this issue of EMBO Molecular Medicine, Decher et al () identify a point mutation in the K2P2 (TREK-1) potassium (K+) channel that changes function in just those ways expected to predispose to right ventricular outflow tract (RVOT) ventricular tachycardia (VT) in the patient they study. Whereas wild-type channels are selective for K+ and inhibited by β-adrenergic stimulation, mutant I267T channels pass sodium (Na+) into the cells, even during β-adrenergic stimulation, and are more active in response to membrane stretch, changes predicted to enhance cardiac myocyte excitability. The report contributes to accumulating evidence for Na+ leak via K2P channels in association with normal development (Thomas et al, 2008), acquired arrhythmia (Ma et al, 2011), and now a missense mutation. Decher et al (2017) both inform and direct us toward interesting opportunities for further investigation.