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The Inward rectifier potassium channel 2.3 (Kir2.3), encoded by the KCNJ4 gene, is a key membrane protein that regulates the flow of potassium ions across cell membranes to maintain the resting membrane potential and control cellular excitability [1, 2]. It is predominantly expressed in the heart and the central nervous system, where it contributes significantly to the terminal phase of action potential repolarization [1]. In cardiac physiology, Kir2.3 is a component of the inward rectifier current (IK1), and its overexpression has been linked to the maintenance of atrial fibrillation by shortening the atrial refractory period [3]. In the brain, Kir2.3 helps modulate neuronal firing and is implicated in the pathophysiology of epilepsy and pain signaling [2, 4]. While specific pharmacological agents for Kir2.3 are currently limited, it is known to be inhibited by non-selective blockers such as barium and certain antiarrhythmic drugs like flecainide [4]. Research into selective Kir2.3 modulators continues as a potential strategy for treating cardiac arrhythmias and neurological disorders, though achieving selectivity over other Kir family members remains a significant challenge [3, 4].
Modulation of the inward rectifier potassium current (IK1) to alter cellular repolarization and resting membrane potential.
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