ArticleIrish journal of medical science2026
miR-646 in early diagnosis and prognostic evaluation of acute myocardial infarction.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundmiR-646 is underexpressed in patients with acute myocardial infarction (AMI), but its clinical diagnostic value and regulatory mechanism remain elusive.
objectiveTo clarify miR-646's clinical significance in AMI and its functional mechanism.
methodsmiR-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.
resultsmiR-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.
conclusionmiR-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.
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