Key result
Transgenic models and pharmacological tools elucidate how cardiac late sodium current drives arrhythmogenesis.
Why the study?
Despite increasing evidence linking late sodium current to dysrhythmia and contractile malfunction, its role in normal and pathologic states remains incompletely understood.
This review outlines the mechanism and function of cardiac late sodium current, highlighting its unquestioned role in arrhythmogenesis and recent advances using transgenic models and pharmacological tools.
Answers are grounded in this paper and cite their sources.
Strengthens mechanistic basis for late sodium current in arrhythmogenesis; leaves open clinical translation of isoform-specific inhibitors.
Late sodium current has long been linked to dysrhythmia and contractile malfunction in the heart. Despite the increasing body of accumulating information on the subject, our understanding of its role in normal or pathologic states is not complete. Even though the role of late sodium current in shaping action potential under physiologic circumstances is debated, it's unquestioned role in arrhythmogenesis keeps it in the focus of research. Transgenic mouse models and isoform-specific pharmacological tools have proved useful in understanding the mechanism of late sodium current in health and disease. This review will outline the mechanism and function of cardiac late sodium current with special focus on the recent advances of the area.
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Horváth et al. (2022) conducted a review in Cardiac dysrhythmia and contractile malfunction. Cardiac late sodium current plays an unquestioned role in arrhythmogenesis, with recent advances utilizing transgenic mouse models and isoform-specific pharmacological tools to elucidate its mechanisms.
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