Zou Shenglan, Li Xiaomin, Liu Xueya, Sun Fei
Department of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou, 225001, China.
Department of Cardiology, DeltaHealth Hospital Shanghai, No.109, Xule Road, Xujing Town, Qingpu District, Shanghai, 201702, China.
J Cardiothorac Surg. 2025 Jun 24;20(1):270. doi: 10.1186/s13019-025-03517-4.
Hypertension is one of the cardiovascular diseases that seriously endangers human life and health, and myocardial hypertrophy is the most common secondary condition of hypertension. Hypertensive with myocardial hypertrophy patients have very high rates of disability and mortality. Previous studies have shown that miR-637 is downregulated in hypertension. Here, our objective was to investigate the correlation and diagnostic potential of serum miR-637 levels in hypertensive patients with myocardial hypertrophy, and to develop new biomarkers for clinical applications.
The content of serum miR-637 was detected by RT-qPCR. ROC curve was used to analyze the diagnostic accuracy of serum miR-637 in hypertension with myocardial hypertrophy. Logistic analysis was used to evaluate the risk factors associated with hypertension with myocardial hypertrophy. The effect of miR-637 on the viability of H9c2 cells was verified by transfection in vitro. The model of myocardial hypertrophy was established by treating H9c2 cells with Ang II.
Compared with healthy controls, miR-637 expression was attenuated in hypertensive patients and weakest in hypertension patients with myocardial hypertrophy. ROC curve showed high sensitivity (78.8%) and specificity (85.0%) of miR-637 in predicting the occurrence of hypertension with myocardial hypertrophy. miR-637 was a risk factor for predicting the development of hypertension with myocardial hypertrophy and showed a negative correlation with LVMI. Overexpression of miR-637 enhanced H9c2 cell viability and decreased apoptosis rate. Ang II treatment decreased miR-637 expression, inhibited cell proliferation, promoted apoptosis, and increased myocardial hypertrophy markers levels, whereas transfection with miR-637 mimic reversed this trend.
miR-637 is poorly expressed in hypertension patients with myocardial hypertrophy and may be an indicator of clinical diagnosis. In addition, miR-637 may serve as a biomarker for diagnosing whether hypertensive patients have myocardial hypertrophy.
高血压是严重危害人类生命健康的心血管疾病之一,心肌肥厚是高血压最常见的继发病症。高血压合并心肌肥厚患者的致残率和死亡率极高。既往研究表明,miR-637在高血压中表达下调。在此,我们的目的是研究血清miR-637水平在高血压合并心肌肥厚患者中的相关性及诊断潜力,并开发用于临床应用的新型生物标志物。
采用RT-qPCR检测血清miR-637的含量。利用ROC曲线分析血清miR-637在高血压合并心肌肥厚中的诊断准确性。采用逻辑回归分析评估与高血压合并心肌肥厚相关的危险因素。通过体外转染验证miR-637对H9c2细胞活力的影响。用血管紧张素II处理H9c2细胞建立心肌肥厚模型。
与健康对照组相比,高血压患者miR-637表达减弱,在高血压合并心肌肥厚患者中最弱。ROC曲线显示,miR-637在预测高血压合并心肌肥厚的发生方面具有较高的敏感性(78.8%)和特异性(85.0%)。miR-637是预测高血压合并心肌肥厚发生的危险因素,且与左心室质量指数呈负相关。miR-637过表达增强了H9c2细胞活力并降低了凋亡率。血管紧张素II处理降低了miR-637表达,抑制细胞增殖,促进凋亡,并增加心肌肥厚标志物水平,而用miR-637模拟物转染可逆转这一趋势。
miR-637在高血压合并心肌肥厚患者中表达较低,可能是临床诊断的一个指标。此外,miR-637可能作为诊断高血压患者是否合并心肌肥厚的生物标志物。