Ablation of Mineralocorticoid Receptors in Myocytes But Not in Fibroblasts Preserves Cardiac Function
Ablation of Mineralocorticoid Receptors in Myocytes But Not in Fibroblasts Preserves Cardiac Function
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DOI：
10.1161/hypertensionaha.110.163287
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发表时间：
2011-04-01
期刊：
影响因子：
8.3
通讯作者：
Hein, Lutz
中科院分区：
文献类型：
--
作者：
Lother, Achim;Berger, Stefan;Hein, Lutz
矿皮质激素受体拮抗剂改善严重心力衰竭患者的发病率和死亡率。然而，参与这些有益作用的细胞类型仅部分为人所知。这项工作的目的是评估小鼠心肌细胞或成纤维细胞中矿皮质激素受体的遗传缺失是否对慢性左心室压力过载后的心脏有保护作用。主动脉横缩后，肌细胞矿化皮质激素受体缺乏的小鼠，而成纤维细胞矿化皮质激素受体缺乏的小鼠，可防止左心室扩张和功能障碍。压力过载后，缺乏肌细胞矿化皮质激素受体的小鼠左心室射血分数（70.2 +/- 4.4%）明显高于对照组小鼠(54.3 +/- 2.5%
Antagonists of the mineralocorticoid receptor improve morbidity and mortality in patients with severe heart failure. However, the cell types involved in these beneficial effects are only partially known. The aim of this work was to evaluate whether genetic deletion of mineralocorticoid receptors in mouse cardiomyocytes or fibroblasts in vivo is cardioprotective after chronic left ventricular pressure overload. After transverse aortic constriction, mice deficient in myocyte mineralocorticoid receptors but not those deficient in fibroblast mineralocorticoid receptors were protected from left ventricular dilatation and dysfunction. After pressure overload, left ventricular ejection fraction was significantly higher in mice lacking myocyte mineralocorticoid receptors (70.2 +/- 4.4%) as compared with control mice (54.3 +/- 2.5%; P