SCN5A: the greatest HITS collection
David S. Park and Glenn I. Fishman
Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, New York, USA.
Address correspondence to: Glenn I. Fishman, Leon H. Charney Division of Cardiology, NYU School of Medicine, 522 First Avenue, Smilow 801, New York, New York 10016, USA. Phone: 212.263.3967; Email: glenn.fishman@nyumc.org.
Find articles by Park, D. in: JCI | PubMed | Google Scholar
Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, New York, USA.
Address correspondence to: Glenn I. Fishman, Leon H. Charney Division of Cardiology, NYU School of Medicine, 522 First Avenue, Smilow 801, New York, New York 10016, USA. Phone: 212.263.3967; Email: glenn.fishman@nyumc.org.
Find articles by Fishman, G. in: JCI | PubMed | Google Scholar
First published February 19, 2018 - More info
J Clin Invest. 2018;128(3):913–915. https://doi.org/10.1172/JCI99927.
Copyright © 2018, American Society for Clinical Investigation
Heart failure (HF) has been referred to as the cardiovascular epidemic of our time. Understanding the molecular determinants of HF disease progression and mortality risk is of utmost importance. In this issue of the JCI, Zhang et al. uncover an important link between clinical HF mortality risk and a common variant that regulates SCN5A expression through microRNA-dependent (miR-dependent)mechanisms. They also demonstrate that haploinsufficiency of SCN5A is associated with increased accumulation of reactive oxygen species (ROS) in a genetically engineered murine model. Their data suggest that even modest depression of SCN5A expression may promote pathologic cardiac remodeling and progression of HF.
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