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首页> 外文期刊>Journal of cardiac failure >Hypertrophy and heart failure in mice overexpressing the cardiac sodium-calcium exchanger.
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Hypertrophy and heart failure in mice overexpressing the cardiac sodium-calcium exchanger.

机译：过度表达心脏钠钙交换剂的小鼠的肥大和心力衰竭。

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BACKGROUND: The cardiac sodium-calcium exchanger (NCX1) is a key sarcolemmal protein for the maintenance of calcium homeostasis in the heart. Because heart failure is associated with increased expression of NCX1, heterozygous (HET) and homozygous (HOM) transgenic mice overexpressing NCX1 were developed and evaluated. METHODS AND RESULTS: The NCX1 transgenic mice display 2.3-fold (HET) and 3.1-fold (HOM) increases in exchanger activity from wild-type (WT) mice. Functional information was obtained by echocardiography and catheterizations before and after hemodynamic stress from pregnancy, treadmill exercise or transaortic constriction (TAC). HET and HOM mice exhibited hypertrophy and blunted responses with beta-adrenergic stimulation. Postpartum mice from all groups were hypertrophied, but only the HOM mice exhibited premature death from heart failure. HOM mice became exercise intolerant after 6 weeks of daily treadmill running. After 21 days TAC, HET, and HOM mice exhibited significant contractile dysfunction and 15% to 40% mortality with clinical evidence of heart failure. CONCLUSIONS: Hemodynamic stress results in a compensated hypertrophy in WT mice, but NCX1 transgenic mice exhibit decreased contractile function and heart failure in proportion to their level of NCX1 expression. Thus exchanger overexpression in mice leads to abnormal calcium handling and a decompensatory transition to heart failure with stress.
机译：背景：心脏钠钙交换剂（NCX1）是维持心脏钙稳态的关键肌膜蛋白。由于心力衰竭与NCX1表达增加有关，因此开发并评估了过表达NCX1的杂合（HET）和纯合（HOM）转基因小鼠。方法和结果：NCX1转基因小鼠与野生型（WT）小鼠相比，交换子活性提高了2.3倍（HET）和3.1倍（HOM）。在妊娠，跑步机运动或经主动脉缩窄（TAC）引起的血流动力学应激前后，通过超声心动图和导管检查获得功能信息。 HET和HOM小鼠在β-肾上腺素刺激下表现出肥大和钝化反应。所有组的产后小鼠都肥大，但只有HOM小鼠表现出因心力衰竭而过早死亡。每天跑步6周后，HOM小鼠变得不耐运动。 21天后，TAC，HET和HOM小鼠表现出明显的收缩功能障碍和15％至40％的死亡率，并伴有心力衰竭的临床证据。结论：血流动力学应激导致野生型小鼠的代偿性肥大，但NCX1转基因小鼠的收缩功能和心力衰竭程度与NCX1表达水平成正比。因此，小鼠中的交换子过度表达会导致钙的异常处理，并导致代偿性向心力衰竭的补偿。

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