Deletion in mice of X‐linked, Brugada syndrome–and atrial fibrillation–associatedKcne5augments ventricular Kvcurrents and predisposes to ventricular arrhythmia

What is it about?

Ion channels are proteins that permit selective movement of ions across the membranes of cells. this movement of ions is used for electrical signaling activity in the body. One example is the beating of the heart, which requires rhythmic, coordinated muscular contraction. This requires coordinated electrical signaling in cardiac muscle cells. KCNE5 is a potassium ion channel regulatory subunit. Variations in the sequence of KCNE5 are linked to cardiac rhythm disturbances (arrhythmia) in humans, including the potentially lethal Brugada syndrome. Here, we genetically deleted Kcne5 from mice to explore possible mechanisms for how Kcne5 disruption causes arrhythmia. We discovered that Kcne5 deletion increases currents through three different types of potassium channel in mouse heart, and also causes arrhythmia in mice. The results can help us explain the role of KCNE5 in the heart, and how KCNE5 sequence variants may cause human cardiac arrhythmia. This can potentially lead to improved treatments.

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