Archives of biochemistry and biophysics · 2025
The role of miR-491-3p in early diagnosis and prognosis evaluation of acute myocardial infarction.
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Dou Tai, Qin Lijie, Zhang Peirong, Xu Lijun, Cheng Yanwei, Wang Peng
Аннотация
AIMS: To investigate the expression characteristics, clinical implications, and underlying mechanisms of miR-491-3p in patients with acute myocardial infarction (AMI).
METHODS: Serum samples were collected from patients with AMI and healthy controls. miR-491-3p expression was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curves evaluated its diagnostic accuracy for AMI. Correlations between miR-491-3p levels and myocardial injury markers or inflammatory factors were analyzed. A one-year follow-up assessed its predictive value for major adverse cardiovascular events (MACE). A hypoxia/reoxygenation (H/R) model of human AC16 cardiomyocytes was established to explore the mechanism of miR-491-3p in H/R-induced injury via targeting aquaporin 9 (AQP9).
RESULTS: Serum miR-491-3p was significantly downregulated in AMI patients, with an AUC of 0.893 for AMI diagnosis (sensitivity 83 %, specificity 79.5 %). Levels were negatively correlated with myocardial injury markers and inflammatory factors. AMI patients with low miR-491-3p expression had a higher incidence of MACE, and low expression was identified as a risk factor. In the H/R model, miR-491-3p was downregulated. Overexpression of miR-491-3p improved cell proliferation, reduced apoptosis, and decreased inflammatory factors by targeting and inhibiting AQP9.
CONCLUSIONS: miR-491-3p may be involved in the pathological process of AMI by targeting and regulating AQP9. This makes it a promising candidate as both a diagnostic and prognostic marker for AMI, as well as a potential therapeutic target.
METHODS: Serum samples were collected from patients with AMI and healthy controls. miR-491-3p expression was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curves evaluated its diagnostic accuracy for AMI. Correlations between miR-491-3p levels and myocardial injury markers or inflammatory factors were analyzed. A one-year follow-up assessed its predictive value for major adverse cardiovascular events (MACE). A hypoxia/reoxygenation (H/R) model of human AC16 cardiomyocytes was established to explore the mechanism of miR-491-3p in H/R-induced injury via targeting aquaporin 9 (AQP9).
RESULTS: Serum miR-491-3p was significantly downregulated in AMI patients, with an AUC of 0.893 for AMI diagnosis (sensitivity 83 %, specificity 79.5 %). Levels were negatively correlated with myocardial injury markers and inflammatory factors. AMI patients with low miR-491-3p expression had a higher incidence of MACE, and low expression was identified as a risk factor. In the H/R model, miR-491-3p was downregulated. Overexpression of miR-491-3p improved cell proliferation, reduced apoptosis, and decreased inflammatory factors by targeting and inhibiting AQP9.
CONCLUSIONS: miR-491-3p may be involved in the pathological process of AMI by targeting and regulating AQP9. This makes it a promising candidate as both a diagnostic and prognostic marker for AMI, as well as a potential therapeutic target.