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.

心力衰竭（HF）被称为我们时代的心血管流行病。了解HF疾病进展和死亡风险的分子决定因素至关重要。在JCI的这一期中，Zhang等人。揭示了临床心衰死亡风险与通过microRNA依赖性（miR依赖性）机制调节SCN5A表达的常见变异之间的重要联系。他们还证明，在基因工程鼠模型中，SCN5A的单倍剂量不足与活性氧（ROS）积累的增加有关。他们的数据表明，即使SCN5A表达的适度降低也可能促进病理性心脏重塑和HF的进展。