ArticleCardiovascular toxicology2021
MiR-124 Regulates the Inflammation and Apoptosis in Myocardial Infarction Rats by Targeting STAT3.
Article in Cardiovascular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The microRNA Expression Profiling in Heart Failure: A Systematic Review and Meta-Analysis.Frontiers in cardiovascular medicine · 2022Pooled it
- Mechanism study of miR-324-3p driving myocardial infarction progression through regulation of myocardial inflammation.Journal of cardiothoracic surgery · 2026Article
- MicroRNA-132 Alleviates Ischemia-Reperfusion-Induced Neuronal Apoptosis by Targeting Mecp2 in Stroke Models.Neurotoxicity research · 2026Article
- Salvianolic acid B protects cardiac function via β3-AR/miRNA-1 axis-mediated cardiomyocyte proliferation in myocardial infarction rats.American journal of translational research · 2026Article
- Extracellular vesicle-derived MicroRNAs as potential therapies for spinal cord and peripheral nerve injuries.RNA biology · 2025Review
- Alpinetin Alleviates Cardiac Inflammation and Remodeling via TLR4/MyD88/NF-κB Signaling Pathway in Rats with Acute Myocardial Infarction.International journal of molecular sciences · 2025Article
- Analysis of Differentially Expressed Murine miRNAs in Acute Myocardial Infarction and Target Genes Related to Heart Rate.Cell biochemistry and biophysics · 2025Article
- Alteration of circulating ACE2-network related microRNAs in patients with COVID-19.Scientific reports · 2024Article
- Unveiling the role of long non-coding RNA MALAT1: a comprehensive review on myocardial infarction.Frontiers in cardiovascular medicine · 2024Review
- Cardiac microRNAs: diagnostic and therapeutic potential.Archives of medical science : AMS · 2023Article
- IL-1β knockdown inhibits cigarette smoke extract-induced inflammation and apoptosis in vascular smooth muscle cells.PloS one · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to discover the effect of miR-124/STAT3 axis on the inflammation and cell apoptosis in myocardial infarction (MI) rats. Sprague-Dawley (SD) male rats were selected for establishing MI models and divided into Sham, MI, MI + anti-miR-124 and MI + Ad-miR-124 groups. Cardiac function was detected via echocardiography. Hematoxylin & eosin (HE) and triphenyltetrazolium chloride (TTC) staining were used to observe the pathological changes and infarction area, while transferase (TdT)-mediated D-UTP-biotin nick end labeling (TUNEL) assay was to observe myocardial apoptosis. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of inflammatory cytokines. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting were performed to determine the mRNA and protein levels, respectively. Dual luciferase reporter gene assay revealed that STAT3 was a target gene of miR-124. The expression levels of miR-124 were increased and the pSTAT3/STAT3 ratio was reduced in the MI rats. The rats in the MI group showed enhanced LVEDD and LVESD, reduced LVEF and LVFS, as well as larger myocardial infarction area compared with the Sham group, Besides, IL-1β, IL-6, TNF-α and MCP-1 levels were elevated and the expressions of Bax/Bcl-2 ratio and cleaved caspase-3 were downregulated in MI group. We further found that silencing miR-124 improved cardiac function, reduced infarction area and the levels of inflammatory cytokines, as well as prevented myocardial apoptosis in MI rats. Silencing miR-124 could inhibit the inflammation and apoptosis of myocardial cells, thereby relieving the MI injury via upregulation of STAT3.
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