Key result
The K2P2 (TREK-1) I267T mutation passes sodium into cells and increases activity in response to membrane stretch, predisposing to right ventricular outflow tract ventricular tachycardia.
Why the study?
Does the K2P2 (TREK-1) I267T mutation alter channel function to predispose to RVOT ventricular tachycardia?
Does the K2P2 (TREK-1) I267T mutation alter channel function to predispose to RVOT ventricular tachycardia?
Answers are grounded in this paper and cite their sources.
The K2P2 (TREK-1) I267T mutation causes sodium leak and altered channel regulation, providing a mechanistic basis for RVOT ventricular tachycardia.
In this issue of EMBO Molecular Medicine , Decher et al (2017) 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.
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Steven A. Goldstein (2017) conducted an editorial in Right ventricular outflow tract (RVOT) ventricular tachycardia (VT). K2P2 (TREK-1) I267T mutation vs. Wild-type channels was evaluated on Sodium leak and cardiac myocyte excitability. The K2P2 (TREK-1) I267T mutation passes sodium into cells and increases activity in response to membrane stretch, predisposing to right ventricular outflow tract ventricular tachycardia.
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