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Updated: Jul 16, 2026
Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
miR-646 in early diagnosis and prognostic evaluation of acute myocardial infarction
Wenhua Wan1, Hongxia Liu2, Wenjing Zhu3
1Coronary Care Unit, Huazhong Fuwai Hospital, Zhengzhou, 450000, China.
Background:
miR-646 is underexpressed in patients with acute myocardial infarction (AMI), but its clinical diagnostic value and regulatory mechanism remain elusive.
Objective:
To clarify miR-646's clinical significance in AMI and its functional mechanism.
Methods:
miR-646 expression was quantified via qRT-PCR. Chi-square and t-tests were used to analyze differences between AMI patients and healthy controls (Ctrl), as well as correlations between MACE and clinical parameters. ROC curve analysis was conducted to evaluate the diagnostic efficacy of miR-646 for AMI, and KM curve analysis was performed to assess its prognostic value for MACE in post-PCI patients. Multivariate Cox regression was used to identify prognostic factors for post-PCI MACE in AMI patients. CCK-8 assays were used to measure cell viability, while flow cytometry was employed to detect cell apoptosis. PIK3R1 was predicted as a miR-646 target and verified by dual-luciferase reporter and RNA pull-down assays.
Results:
miR-646 expression was significantly lower in AMI patients than in Ctrl, and in post-PCI MACE patients than in non-MACE counterparts. Reduced miR-646 expression serves as an AMI diagnostic indicator and links to higher post-PCI MACE risk. miR-646, cTnI, CK-MB, and LVEF were identified as factors for post-PCI MACE in AMI patients. miR-646 upregulation significantly restored the viability of hypoxic AC16 cells and inhibited their apoptosis. PIK3R1 overexpression reversed the pro-viability and anti-apoptotic effects induced by miR-646 mimic.
Conclusion:
miR-646 may serve as a diagnostic biomarker for AMI and a predictor of MACE in post-PCI AMI patients, with its mechanism linked to targeted PIK3R1 regulation.
Insights
MicroRNA-646 (miR-646) is underexpressed in acute myocardial infarction (AMI) patients and predicts major adverse cardiac events (MACE) after percutaneous coronary intervention (PCI). Its mechanism involves targeting PIK3R1, offering diagnostic and prognostic potential.
Area of Science:
- Cardiovascular Biology
- Molecular Diagnostics
- Biomarker Discovery
Background:
- MicroRNA-646 (miR-646) is underexpressed in acute myocardial infarction (AMI).
- The clinical diagnostic value and regulatory mechanism of miR-646 in AMI are not well understood.
Purpose of the Study:
- To investigate the clinical significance of miR-646 in AMI.
- To elucidate the functional mechanism of miR-646 in AMI and its association with major adverse cardiac events (MACE) post-percutaneous coronary intervention (PCI).
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for miR-646 expression analysis.
- Statistical analyses including Chi-square, t-tests, ROC curve, and KM curve analysis.
- Cell viability (CCK-8) and apoptosis (flow cytometry) assays; dual-luciferase reporter and RNA pull-down assays to verify PIK3R1 as a miR-646 target.
Main Results:
- miR-646 expression was significantly lower in AMI patients and in post-PCI MACE patients.
- Reduced miR-646 expression is a diagnostic indicator for AMI and predicts higher MACE risk post-PCI.
- miR-646 upregulation restored cell viability and inhibited apoptosis in hypoxic cells, an effect reversed by PIK3R1 overexpression.
Conclusions:
- miR-646 shows potential as a diagnostic biomarker for AMI.
- miR-646 can predict MACE in AMI patients undergoing PCI.
- The mechanism involves miR-646 targeting PIK3R1, influencing cell viability and apoptosis.
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