Heart often undergoes mal-remodeling and hypertrophic growth in response to pathological stress. MiRNAs can regulate the cardiac function and participate in the regulation of cardiac hypertrophy. The present study aims at identifying the role of miR-296-5p in cardiac hypertrophy and further the underlying mechanism in hypertrophic cascades. Mice with cardiac hypertrophy were established by transverse aortic constriction (TAC). Cardiac hypertrophy in cardiomyocytes was induced by angiotensin II. Expression of miR-296-5p and its target gene CACNG6 was examined in cardiomyocytes transfected by miRNA. The expression of miR-296-5p was upregulated in mice with TAC surgery. The inhibition of miR-296-5p attenuated cardiac hypertrophy both in vitro and in vivo. And dual-luciferase reporter assays showed CACNG6 was the direct target of miR-296-5p, which modulated the expression of calcium signaling. MiR-296-5p was found to aggravate cardiac hypertrophy by targeting CACNG6, which suggests inhibition of miR-296-5p might have clinical potential to suppress cardiac hypertrophy and heart failure.

中文翻译：

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撤回文章：抑制 miR-296-5p 通过靶向 CACNG6 保护心脏免受心脏肥大。

心脏通常会因病理性应激而发生重塑不良和肥大性生长。miRNAs可以调节心脏功能，参与心肌肥厚的调节。本研究旨在确定 miR-296-5p 在心脏肥大中的作用，并进一步探讨肥大级联反应的潜在机制。通过横向主动脉缩窄术 (TAC) 建立具有心脏肥大的小鼠。心肌细胞的心肌肥大是由血管紧张素 II 诱导的。在 miRNA 转染的心肌细胞中检查 miR-296-5p 及其靶基因 CACNG6 的表达。在接受 TAC 手术的小鼠中，miR-296-5p 的表达上调。抑制 miR-296-5p 可在体外和体内减弱心脏肥大。双荧光素酶报告基因检测显示 CACNG6 是 miR-296-5p 的直接靶标，调节钙信号的表达。发现 MiR-296-5p 通过靶向 CACNG6 加重心脏肥大，这表明抑制 miR-296-5p 可能具有抑制心脏肥大和心力衰竭的临床潜力。