Heart failure is a major cardiovascular disease, characterized by considerable morbidity and mortality. Despite major advances in the pharmacotherapy of heart failure, the options for patients with severe end-stage symptoms remain limited. However, recent developments in the identification of the molecular basis for the progressive nature of heart failure have identified a number of potentially important new therapeutic targets. In particular, key components of the cardiomyocyte calcium-handling pathway show characteristic changes in heart failure. A body of research examining the effect of restoration of these defects in experimental models of heart failure, whether in genetically engineered mouse models or by myocardial gene transfer, very strongly supports the calcium-handling pathway as a target for clinical intervention.

中文翻译：

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通过靶向Ca2 +循环来逆转晚期心力衰竭。

心力衰竭是一种主要的心血管疾病，其特征是发病率和死亡率都很高。尽管心力衰竭的药物治疗取得了重大进展，但对于具有严重终末期症状的患者的选择仍然有限。然而，心力衰竭进行性的分子基础鉴定的最新进展已经鉴定出许多潜在重要的新治疗靶标。特别是，心肌细胞钙处理途径的关键组成部分表现出心力衰竭的特征性变化。一项研究在心力衰竭的实验模型中，无论是在基因工程小鼠模型中还是在心肌基因转移中，对这些缺陷的修复效果进行了研究，都强烈支持将钙处理途径作为临床干预的目标。