The Department of Cardiology, Dongguan People's Hospital, Dongguan, Guangdong, China.
Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
J Biochem Mol Toxicol. 2022 Aug;36(8):e23093. doi: 10.1002/jbt.23093. Epub 2022 May 5.
Heart failure is a condition caused by a variety of pathophysiological factors. One important pathological change of chronic heart failure is myocardial hypertrophy. In recent years, several studies have found that dysregulated microRNAs are involved in regulating the pathological process of heart failure. In this study, cardiac hypertrophy models were constructed using isoproterenol (ISO)-/angiotensin-II (Ang-II) to explore the role of miR-384-5p in cardiac hypertrophy and its molecular mechanism in vivo and in vitro. Echocardiography, invasive pressure-volume analysis and hematoxylin-eosin staining were used to explore cardiac structure and function. ALPK3 mRNA and protein expression were detected using quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot analysis and miR-384-5p expression were assessed via RT-qPCR. Our findings determined that miR-384-5p was notably decreased in cardiac hypertrophic tissues and cells, and overexpression of miR-384-5p could ameliorate pressure overload. Furthermore, ALPK3 was determined to downregulate the ALPK3 expression to aggravate cardiomyocyte hypertrophy. Our findings provided a potential therapeutic target for the treatment of cardiac hypertrophy.
心力衰竭是由多种病理生理因素引起的一种病症。慢性心力衰竭的一个重要病理变化是心肌肥厚。近年来，有几项研究发现，失调的 microRNA 参与调节心力衰竭的病理过程。在这项研究中，使用异丙肾上腺素（ISO）/血管紧张素-II（Ang-II）构建心肌肥厚模型，以在体内和体外探索 miR-384-5p 在心肌肥厚中的作用及其分子机制。通过超声心动图、侵入性压力-容积分析和苏木精-伊红染色来探索心脏结构和功能。通过定量逆转录聚合酶链反应（RT-qPCR）和 Western blot 分析检测 ALPK3 mRNA 和蛋白表达，通过 RT-qPCR 评估 miR-384-5p 的表达。我们的研究结果表明，miR-384-5p 在心肌肥厚组织和细胞中明显减少，过表达 miR-384-5p 可以改善压力超负荷。此外，ALPK3 被确定下调 ALPK3 表达以加重心肌细胞肥大。我们的研究结果为治疗心肌肥厚提供了一个潜在的治疗靶点。
