Sodium leak through K2P potassium channels and cardiac arrhythmia, an emerging theme
| Autor: | Steve A.N. Goldstein |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Sodium chemistry.chemical_element Stimulation Ventricular tachycardia Cardiovascular System 03 medical and health sciences Potassium Channels Tandem Pore Domain Internal medicine medicine Ventricular outflow tract Missense mutation Humans News & Views Chemistry Cardiac myocyte Cardiac arrhythmia Middle Aged medicine.disease Potassium channel 3. Good health 030104 developmental biology Endocrinology Cardiology Tachycardia Ventricular Molecular Medicine Mutant Proteins Genetics Gene Therapy & Genetic Disease |
| Zdroj: | EMBO Molecular Medicine |
| ISSN: | 1757-4684 1757-4676 |
| Popis: | In this issue of EMBO Molecular Medicine , Decher et al ([2017][1]) 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][2]), acquired arrhythmia (Ma et al , [2011][3]), and now a missense mutation. Decher et al ([2017][1]) both inform and direct us toward interesting opportunities for further investigation. [1]: #ref-4 [2]: #ref-11 [3]: #ref-8 |
| Databáze: | OpenAIRE |
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