Myostatin does not regulate cardiac hypertrophy or fibrosis
Myostatin does not regulate cardiac hypertrophy or fibrosis
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DOI：
10.1016/j.nmd.2007.01.011
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发表时间：
2007-04-01
影响因子：
2.8
通讯作者：
Wagner, Kathryn R.
中科院分区：
文献类型：
--
作者：
Cohn, Ronald D.;Liang, Hsin-Yueh;Wagner, Kathryn R.
肌肉生长抑制素是肌肉生长的负调节剂。在肌营养不良蛋白缺陷型 mdx 肌营养不良症小鼠模型中，肌生长抑制素的缺失已被证明会导致骨骼肌尺寸增加，并改善骨骼肌功能和纤维化。我们评估了肌生长抑制素的缺乏是否对体内心肌生长和纤维化有影响。使用转基因小鼠，我们评估了肌生长抑制素的缺失是否会对心脏功能和纤维化产生类似的有益影响。通过高分辨率超声心动图测量野生型、肌生长抑制素缺失、mdx 和双突变 mdx/肌生长抑制素缺失小鼠的心脏质量和射血分数。死后测定心脏质量、肌细胞面积和心脏纤维化程度。与野生型小鼠相比，无肌生长抑制素的小鼠没有表现出心室肥大，如超声心动图（心室质量 0.69 +/- 0.01 vs. 0.69 +/- 0.018 g）和形态测量分析（包括心脏/体重比（5.39 +/- 0.45 vs. 5.62 +/- 0.58 mg/g）和心肌细胞面积 113.67 +/-）所示。 1.5, 116.85 +/- 1.9 微米(2))。此外，缺乏肌生长抑制素并不能减轻肌营养不良蛋白缺陷 mdx 小鼠的心脏纤维化（12.2% vs. 12%）。肌生长抑制素在心肌中的生理作用与在骨骼肌中的生理作用明显不同，因为它不会诱导 mdx 小鼠心脏肥大，也不会调节心脏纤维化。 (c) 2007 Elsevier B.V. 保留所有权利。
Myostatin is a negative regulator of muscle growth. Loss of myostatin has been shown to cause increase in skeletal muscle size and improve skeletal muscle function and fibrosis in the dystrophin-deficient mdx muscular dystrophy mouse model. We evaluated whether lack of myostatin has an impact on cardiac muscle growth and fibrosis in vivo. Using genetically modified mice we assessed whether myostatin absence induces similar beneficial effects on cardiac function and fibrosis. Cardiac mass and ejection fraction were measured in wild-type, myostatin-null, mdx and double mutant mdx/myostatin-null mice by high resolution echocardiography. Heart mass, myocyte area and extent of cardiac fibrosis were determined post mortem. Myostatin-null mice do not demonstrate ventricular hypertrophy when compared to wild-type mice as shown by echocardiography (ventricular mass 0.69 +/- 0.01 vs. 0.69 +/- 0.018 g) and morphometric analyses including heart/body weight ratio (5.39 +/- 0.45 vs. 5.62 +/- 0.58 mg/g) and cardiomyocyte area 113.67 +/- 1.5, 116.85 +/- 1.9 mu m(2)). Moreover, absence of myostatin does not attenuate cardiac fibrosis in the dystrophin-deficient mdx mouse (12.2% vs. 12%). The physiological role of myostatin in cardiac muscle appears significantly different than that in skeletal muscle as it does not induce cardiac hypertrophy and does not modulate cardiac fibrosis in mdx mice. (c) 2007 Elsevier B.V. All rights reserved.