ArticleHereditas2026
miR-146b-5p serves as a novel biomarker for acute myocardial infarction and is involved in regulating oxidized low-density lipoprotein-induced endothelial injury through targeting PRKAR2A.
Article in Hereditas, 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-146b-5p, a disease-responsive miRNA with circulatory stability, has been implicated in multiple pathologies, but its role in acute myocardial infarction (AMI) remains unexplored. The objective of this study was to explore the role of miR-146b-5p in AMI.
methodsSerum from 103 AMI patients and 95 healthy controls was analyzed via qRT-PCR to quantify miR-146b-5p/PRKAR2A expression, with ROC curves evaluating diagnostic performance and correlation analyses linking miR-146b-5p levels to clinical indicators of AMI severity. Prognostic associations were systematically assessed using Kaplan-Meier curves and COX regression models. In vitro ox-LDL-induced HCAEC injury models employed CCK-8 assays, flow cytometry, Caspase-3 activity measurements, ELISA, and oxidative stress assays to elucidate cellular mechanisms. Dual-luciferase reporter and Western blot assays assessed the relation between miR-146b-5p and PRKAR2A.
resultsUpregulated miR-146b-5p expression was observed in AMI compared with the HC group, showing diagnostic value and correlation with hs-CRP, CK-MB, cTnI, LVEF, and Killip grade. Higher miR-146b-5p expression predicted poor prognosis of AMI. In ox-LDL-induced HCAECs, miR-146b-5p inhibition reduced apoptosis, inflammation (IL-1β, TNF-α), and endothelial dysfunction marker levels (ET-1, vWF), while promoting proliferation. PRKAR2A was downregulated in ox-LDL and confirmed as a miR-146b-5p target, with its knockdown reversing the protective effects of miR-146b-5p inhibition on ox-LDL-induced HCAEC injury.
conclusionsUpregulated miR-146b-5p, which correlated with AMI severity, demonstrated diagnostic and prognostic potential for AMI. It promoted AMI progression by aggravating endothelial injury under ox-LDL induction through suppressing PRKAR2A.
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