As a strong transactivator of promoters containing CarG boxes, myocardin was critical for the cardiac muscle program and necessary for normal cardiogenesis. So it probably represents a viable therapeutic biomarker in the setting of cardiac hypertrophy and failure. In recent years, the studies of regulation of cardiac hypertrophy via myocardin are so common, and the molecular mechanism is becoming more and more clear. Here, we have revealed a kind of interaction between mhrt and myocardin shown as a feedback regulatory mechanism in the regulation of cardiac hypertrophy. That is, the lncRNA mhrt can affect the acetylation of myocardin by HDAC5 to inhibit cardiac hypertrophy induced by myocardin. Moreover, myocardin also can directly activate the mhrt transcription through binding to the CarG box. Thus, mhrt and myocardin form a regulation loop in the process of cardiac hypertrophy. This finding may play a positive role in revealing the complete mechanisms of cardiac hypertrophy.

作为含有CarG盒的启动子的强反式激活剂，心肌素对于心肌程序至关重要，对于正常的心脏发生是必不可少的。因此，在心脏肥大和衰竭的情况下，它可能代表了可行的治疗性生物标志物。近年来，通过心肌调节心肌肥大的研究非常普遍，其分子机制也越来越清晰。在这里，我们揭示了mhrt和心肌素之间的一种相互作用，显示为心脏肥大调节中的一种反馈调节机制。也就是说，lncRNA mhrt可以影响HDAC5对心肌素的乙酰化作用，从而抑制由心肌素引起的心肌肥大。此外，心肌素还可以通过与CarG盒结合而直接激活mhrt转录。因此，mhrt和心肌素在心脏肥大过程中形成一个调节环。这一发现可能在揭示心脏肥大的完整机制中起积极作用。