Key result
Lower serum miR-637 linked to myocardial hypertrophy in hypertensive patients with an AUC of ~0.88.
Why the study?
Hypertensive patients with myocardial hypertrophy have high disability and mortality rates, and previous studies showed miR-637 is downregulated in hypertension.
Does serum miR-637 level predict the occurrence of myocardial hypertrophy in patients with hypertension?
Case-Control (n=240)
No
Does serum miR-637 level predict the occurrence of myocardial hypertrophy in patients with hypertension?
Odds Ratio: 0.075 (95% CI 0.027–0.207)
p-value: p=<0.001
Serum miR-637 is downregulated in hypertensive patients with myocardial hypertrophy and may serve as a diagnostic biomarker.
Low miR-637 was associated with hypertensive myocardial hypertrophy; leaves open prospective validation before diagnostic use.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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Zou et al. (2025) conducted a case-control in Hypertension with myocardial hypertrophy (n=240). Serum miR-637 vs. Healthy controls and hypertensive patients without myocardial hypertrophy was evaluated on Occurrence of hypertension with myocardial hypertrophy (OR 0.075, 95% CI 0.027-0.207, p=<0.001). Lower serum miR-637 levels were significantly associated with the occurrence of myocardial hypertrophy in hypertensive patients (OR 0.075), demonstrating high diagnostic accuracy with an AUC of 0.881.
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