Key result
Inhibition of NaV1.8 decreased persistent Na+ current, abbreviated action potential duration, and reduced cellular-spontaneous Ca2+-release and proarrhythmic events in failing cardiomyocytes.
Why the study?
Does NaV1.8 inhibition reduce proarrhythmic cellular events in failing cardiomyocytes?
Population
Human failing cardiomyocytes and mouse cardiomyocytes
Comparison
NaV1.8 inhibition vs Control/untreated cardiomyocytes
Design
Preclinical
Authors
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NaV1.8 expression in failing hearts supports further target validation; leaves open whether selective inhibition reduces arrhythmias.
Does NaV1.8 inhibition reduce proarrhythmic cellular events in failing cardiomyocytes?
NaV1.8 is upregulated in human heart failure and its inhibition reduces proarrhythmic events, suggesting a novel target for anti-arrhythmic therapy.
Dybkova et al. (2018) studied Heart failure. NaV1.8 inhibition (A-803467, PF-01247324, and SCN10A-/-) was evaluated on Persistent Na+ current (INaL), action potential duration (APD), Ca2+ spark frequency, and arrhythmia induction. Inhibition of NaV1.8 decreased persistent Na+ current, abbreviated action potential duration, and reduced cellular-spontaneous Ca2+-release and proarrhythmic events in failing cardiomyocytes.
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