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May guide arrhythmia mechanism research; leaves open targeted therapy development for trafficking defects.
Electrical excitability in cells such as neurons and myocytes depends not only upon the expression of voltage-gated sodium channels but also on their correct targeting within the plasma membrane. Placing sodium channels within a broader cell biological context is beginning to shed new light on a variety of important questions such as the integration of neuronal signaling. Mutations that affect sodium channel trafficking have been shown to underlie several life-threatening conditions including cardiac arrhythmias, revealing an important clinical context to these studies.
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Cusdin et al. (2007) studied this question.
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