Cardiac hypertrophy is an adaptive response to manage an excessive cardiac workload and maintain normal cardiac function. However, sustained hypertrophy leads to cardiomyopathy, cardiac failure, and death. Adrenergic receptors play a key role in regulating cardiac function under normal and pathological conditions. Mitochondria are responsible for 90% of ATP production in cardiomyocytes. Mitochondrial function is dynamically regulated by fusion and fission processes. Changes in mitochondrial dynamics and metabolism are central issues in cardiac hypertrophy. Stimulating cardiomyocytes with adrenergic agonists generates hypertrophy and increases mitochondrial fission, which in turn is associated with decreased ATP synthesis. Miro1 is a mitochondrial outer membrane protein involved in mitochondrial dynamics and transport in neurons. The objective of this work was to evaluate whether Miro1 regulates cardiomyocyte hypertrophy through changes in mitochondrial dynamics. In neonatal rat ventricular myocytes, we showed that phenylephrine induced cardiomyocyte hypertrophy and increased Miro1 mRNA and protein levels. Moreover, alpha-adrenergic stimulation provoked a mitochondrial fission pattern in the cardiomyocytes. Miro1 knockdown prevented both the cardiomyocyte hypertrophy and mitochondrial fission pattern. Our results suggest that Miro1 participates in phenylephrine-induced cardiomyocyte hypertrophy through mitochondrial fission.

中文翻译：

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Miro1作为新生大鼠心肌细胞肥大的新型调节剂。

心脏肥大是适应性反应，可处理过多的心脏工作量并维持正常的心脏功能。然而，持续的肥大导致心肌病，心力衰竭和死亡。肾上腺素能受体在正常和病理情况下在调节心脏功能中起关键作用。线粒体负责心肌细胞中90％的ATP产生。线粒体功能由融合和裂变过程动态调节。线粒体动力学和代谢的变化是心脏肥大的核心问题。用肾上腺素能激动剂刺激心肌细胞产生肥大并增加线粒体裂变，这又与ATP合成减少有关。Miro1是一种线粒体外膜蛋白，参与神经元的线粒体动力学和转运。这项工作的目的是评估Miro1是否通过线粒体动力学变化来调节心肌肥大。在新生大鼠心室肌细胞中，我们显示去氧肾上腺素诱导心肌肥大并增加Miro1 mRNA和蛋白质水平。此外，α-肾上腺素刺激引起心肌细胞的线粒体裂变模式。Miro1组合式可防止心肌肥大和线粒体裂变模式。我们的结果表明，Miro1通过线粒体裂变参与了去氧肾上腺素诱导的心肌肥大。我们显示去氧肾上腺素诱导心肌肥大并增加Miro1 mRNA和蛋白质水平。此外，α-肾上腺素刺激引起心肌细胞的线粒体裂变模式。Miro1组合式可防止心肌肥大和线粒体裂变模式。我们的结果表明，Miro1通过线粒体裂变参与了去氧肾上腺素诱导的心肌肥大。我们显示去氧肾上腺素诱导心肌肥大并增加Miro1 mRNA和蛋白质水平。此外，α-肾上腺素刺激引起心肌细胞的线粒体裂变模式。Miro1组合式可防止心肌肥大和线粒体裂变模式。我们的结果表明，Miro1通过线粒体裂变参与了去氧肾上腺素诱导的心肌肥大。