ArticleCardiovascular research2017
Therapeutic inhibition of miR-375 attenuates post-myocardial infarction inflammatory response and left ventricular dysfunction via PDK-1-AKT signalling axis.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells.Frontiers in cell and developmental biology · 2020Pooled it
- Muscle-specific miR-499-5p delivered by small extracellular vesicles impairs endothelial function and ischemic hindlimb recovery in diabetic mice.Cardiovascular diabetology · 2025Article
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- GPC3-mediated metabolic rewiring of diabetic mesenchymal stromal cells enhances their cardioprotective functions via PKM2 activation.iScience · 2024Article
- Epigenetic regulation of sex dimorphism in cardiovascular health.Canadian journal of physiology and pharmacology · 2024Review
- Inhibition of Pyruvate Dehydrogenase Kinase 4 Protects Cardiomyocytes from lipopolysaccharide-Induced Mitochondrial Damage by Reducing Lactate Accumulation.Inflammation · 2024Article
- MicroRNA delivery based on nanoparticles of cardiovascular diseases.Molecular and cellular biochemistry · 2024Review
- Tipifarnib Reduces Extracellular Vesicles and Protects From Heart Failure.Circulation research · 2024Article
- miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach.International journal of molecular sciences · 2023Review
- SARS-CoV-2-associated organs failure and inflammation: a focus on the role of cellular and viral microRNAs.Virology journal · 2023Review
- New Insights into the Reparative Angiogenesis after Myocardial Infarction.International journal of molecular sciences · 2023Review
- Heart failure with preserved ejection fraction and non-alcoholic fatty liver disease: new insights from bioinformatics.ESC heart failure · 2023Article
- Epigenetic Regulation of Macrophage Polarization in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Exosome-Encapsulated miR-31, miR-192, and miR-375 Serve as Clinical Biomarkers of Gastric Cancer.Journal of oncology · 2023Article
- Extracellular vesicles mediate biological information delivery: A double-edged sword in cardiac remodeling after myocardial infarction.Frontiers in pharmacology · 2023Review
- Bioinformatics analysis identifies ferroptosis‑related genes in the regulatory mechanism of myocardial infarction.Experimental and therapeutic medicine · 2022Article
- Cell-Based and Selected Cell-Free Therapies for Myocardial Infarction: How Do They Compare to the Current Treatment Options?International journal of molecular sciences · 2022Review
- Article
- Review
- Hsa-miR-199a-5p Protect Cell Injury in Hypoxia Induces Myocardial Cells Via Targeting HIF1α.Molecular biotechnology · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
aimsIncreased miR-375 levels has been implicated in rodent models of myocardial infarction (MI) and with patients with heart failure. However, no prior study had established a therapeutic role of miR-375 in ischemic myocardium. Therefore, we assessed whether inhibition of MI-induced miR-375 by LNA anti-miR-375 can improve recovery after acute MI. METHODS AND
resultsTen weeks old mice were treated with either control or LNA anti miR-375 after induction of MI by LAD ligation. The inflammatory response, cardiomyocyte apoptosis, capillary density and left ventricular (LV) functional, and structural remodelling changes were evaluated. Anti-miR-375 therapy significantly decreased inflammatory response and reduced cardiomyocyte apoptosis in the ischemic myocardium and significantly improved LV function and neovascularization and reduced infarct size. Repression of miR-375 led to the activation of 3-phosphoinositide-dependent protein kinase 1 (PDK-1) and increased AKT phosphorylation on Thr-308 in experimental hearts. In corroboration with our in vivo findings, our in vitro studies demonstrated that knockdown of miR-375 in macrophages modulated their phenotype, enhanced PDK-1 levels, and reduced pro-inflammatory cytokines expression following LPS challenge. Further, miR-375 levels were elevated in failing human heart tissue.
conclusionTaken together, our studies demonstrate that anti-miR-375 therapy reduced inflammatory response, decreased cardiomyocyte death, improved LV function, and enhanced angiogenesis by targeting multiple cell types mediated at least in part through PDK-1/AKT signalling mechanisms.
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