Cardiac hypertrophy is an adaptive response to hemodynamic stress to compensate for cardiac dysfunction. MicroRNAs can regulate cardiac function and play a vital role in the regulation of cardiac hypertrophy. In the current study, in vivo and vitro hypertrophy models are established to explore the role of miR-27b and to elucidate the underlying mechanism in cardiac hypertrophy. Expression of miR-27b was down-regulated in mice with cardiac hypertrophy. The cardiac function of the mice with cardiac hypertrophy could be restored with the overexpression of miR-27b, this is observed in terms of decreasing LVEDd, LVESd, and increasing LVFS, LVEF. This study also predicted and confirmed that galectin-3 is a target gene of miR-27b. Depletion of galectin-3 significantly attenuated hypertrophy of hearts in both in vitro and in vivo tests. In conclusion, MiR-27b be used to exert a protective role against cardiac dysfunction and hypertrophy by decreasing the expression level of galectin-3. The methodology suggested in this study provides a novel therapeutic strategy against cardiac hypertrophy.

心脏肥大是对血流动力学压力的适应性反应，以补偿心脏功能障碍。MicroRNA可以调节心脏功能，并在心脏肥大的调节中起重要作用。在当前研究中，建立了体内和体外肥大模型，以探索miR-27b的作用并阐明心肌肥大的潜在机制。在患有心肌肥大的小鼠中，miR-27b的表达下调。miR-27b的过表达可以恢复具有心脏肥大的小鼠的心脏功能，这可以通过降低LVEDd，LVESd和增加LVFS，LVEF来观察。该研究还预测并证实了galectin-3是miR-27b的靶基因。在体外和体内测试中，galectin-3的耗竭显着减弱了心脏的肥大。结论，通过降低Galectin-3的表达水平，MiR-27b可发挥抗心脏功能障碍和肥大的保护作用。这项研究中建议的方法提供了一种针对心脏肥大的新颖治疗策略。