ArticleCardiovascular toxicology2024
miRNA-146a-5p Inhibits Hypoxia-Induced Myocardial Fibrosis Through EndMT.
Article in Cardiovascular toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Decoding miRNA‑146a: Mechanisms of action in cardiovascular diseases and endocrine metabolic disorders (Review).International journal of molecular medicine · 2026Review
- Advances in MicroRNA-Based Therapies for Cardiac Repair: Emerging Strategies for Treating Myocardial Infarction.Molecular and cellular biochemistry · 2026Review
- Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis.Frontiers in cell and developmental biology · 2026Review
- CircIdh2 Attenuates Endothelial-to-Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential.Cardiovascular therapeutics · 2026Article
- Electroacupuncture preconditioning alleviates myocardial ischemia-reperfusion injury through reducing the inflammatory response mediated by the miR-146a/TRAF6/IRAK4 pathway.Iranian journal of basic medical sciences · 2026Article
- MicroRNA Signatures in Cardiometabolic Disorders as a Next-Generation Diagnostic Approach: Current Insight.International journal of molecular sciences · 2025Review
- miR-17-5p Inhibits BNIP3-Mediated Mitochondrial Autophagy to Attenuate Pathological Cardiac FibrosisBalkan medical journal · 2025Article
- Ginsenoside Rb1 inhibits M1 macrophages-induced IGFBP2-mediated endothelial-mesenchymal transition to alleviate myocardial fibrosis in mice with chronic heart failure.In vitro cellular & developmental biology. Animal · 2025Article
- Mechanistic insights and emerging therapeutic strategies targeting endothelial dysfunction in cardiovascular diseases.Archives of pharmacal research · 2025Review
- Diagnostic and Predictive Value of LncRNA MCM3AP-AS1 in Sepsis and Its Regulatory Role in Sepsis-Induced Myocardial Dysfunction.Cardiovascular toxicology · 2024Article
- Targeting delivery of miR-146a via IMTP modified milk exosomes exerted cardioprotective effects by inhibiting NF-κB signaling pathway after myocardial ischemia-reperfusion injury.Journal of nanobiotechnology · 2024Article
- miR-652-3p Suppressed the Protective Effects of Isoflurane Against Myocardial Injury in Hypoxia/Reoxygenation by Targeting ISL1.Cardiovascular toxicology · 2024Article
- EMMPRIN promotes spheroid organization and metastatic formation: comparison between monolayers and spheroids of CT26 colon carcinoma cells.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac Vascular disease particularly myocardial infarction (MI) is a threat to health worldwide. microRNAs (miRNAs) have been shown to regulate myocardial fibrosis. Therefore, it is potential to investigate the mechanism of miRNA and fibrosis following myocardial infarction. Hypoxia human cardiac microvascular endothelial cells (HCMECs) were selected for the vitro experimental model. The miR-146a-5p expression was tested via RT-qPCR. The level of endothelial-to-mesenchymal transition (EndMT) and fibrosis markers were detected by Western blotting and immunofluorescence. Then, the inflammation, cell viability and apoptosis were investigated. The target was predicted by an online database and verified by a dual-luciferase activity assay. An MI mouse model was created to validate that miR-146a-5p regulates cardiac fibrosis in vivo. MI mouse was transfected with miR-146a-5p lentivirus. Subsequently, its effect on cardiac fibrosis of infarcted hearts was assessed by In situ hybridization (ISH), Immunohistochemistry (IHC), Triphenylterazolium chloride (TTC) staining and Masson staining. Herein, we confirmed that miR-146a-5p was down-regulated in hypoxia HCMECs. Overexpression of miR-146a-5p inhibited hypoxia-induced cardiac fibrosis following myocardial infarction by inhibiting EndMT in HCMECs. Thioredoxin-interacting protein (TXNIP) was a target that was negatively regulated by miR-146a-5p. Up-regulation of miR-146a-5p inhibited cardiac fibrosis via regulating EndMT by targeting TXNIP, and it also regulated EndMT to inhibit cardiac fibrosis in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.