What is it about?
This Editorial on the work by Luo and colleagues (https://doi.org/10.1111/apha.12872) discusses potential mechanisms trying to explain altered function of the cardiac voltage-gated sodium (NaV) channel in heart failure, a pathology taking place when the heart cannot pump and maintain the blood flow adequately.
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Why is it important?
How heart failure arises is not well understood. The paper discussed proposes that increased cellular calcium affects functioning of NaV1.5 (the cardiac NaV channel). They propose an intriguing link between cellular sodium imbalance as a cause of alterations in calcium channel transport, in turn leading to subsequent defects on NaV1.5 levels and functioning.
Perspectives
The findings from that work are interesting since open a possible link between cellular calcium levels and altered sodium current in heart failure via NaV1.5 regulation. This adds not only to the understanding of mechanisms causing heart failure, but could also contribute to devising potential new treatments.
Dr Marcel Verges
University of Girona
Read the Original
This page is a summary of: A mechanism for NaV
1.5 downregulation and sodium current decrease in heart failure, Acta Physiologica, June 2017, Wiley,
DOI: 10.1111/apha.12901.
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