ArticleOxidative medicine and cellular longevity2021
miRNA-146a Mimic Inhibits NOX4/P38 Signalling to Ameliorate Mouse Myocardial Ischaemia Reperfusion (I/R) Injury.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Decoding miRNA‑146a: Mechanisms of action in cardiovascular diseases and endocrine metabolic disorders (Review).International journal of molecular medicine · 2026Review
- Biomimetic Bone Marrow Monocyte Membrane-Fused Extracellular Vesicles for Targeted Therapy of Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Synthetically designed circRNA can be used to target cardiovascular relevant microRNAs to improve cellular function.Scientific reports · 2026Article
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- The Dual Role of NOX4 in Cardiovascular Diseases: Driver of Oxidative Stress and Mediator of Adaptive Remodeling.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- A Thorough Navigation of miRNA's Blueprint in Crafting Cardiovascular Fate.Health science reports · 2024Article
- Unveiling the therapeutic potential of miR-146a: Targeting innate inflammation in atherosclerosis.Journal of cellular and molecular medicine · 2024Review
- 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-146a Decreases Inflammation and ROS Production in Aged Dermal Fibroblasts.International journal of molecular sciences · 2024Article
- Impaired regulation of MMP2/16-MLCK3 by miR-146a-5p increased susceptibility to myocardial ischaemic injury in aging mice.Cardiovascular research · 2023Article
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Metallothionein-2A Protects Cardiomyocytes from Hypoxia/reper-Fusion through Inhibiting p38.Cell biochemistry and biophysics · 2023Article
- Inflammatory microRNAs in cardiovascular pathology: another brick in the wall.Frontiers in immunology · 2023Review
- microRNAs as biomarkers of risk of major adverse cardiovascular events in atrial fibrillation.Frontiers in cardiovascular medicine · 2023Review
- Mechanisms and application strategies of miRNA‑146a regulating inflammation and fibrosis at molecular and cellular levels (Review).International journal of molecular medicine · 2023Review
- Yin and Yang of NADPH Oxidases in Myocardial Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2022Review
- Research progress in endothelial cell injury and repair.Frontiers in pharmacology · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence suggests that miR-146a is implicated in the pathogenesis of cardiovascular diseases; however, the role of miR-146a in myocardial ischaemia reperfusion (I/R) injury is unclear. The aim of this study was to explore the functional role of miR-146a in myocardial ischaemia reperfusion injury and the underlying mechanism. C57BL/6J mice were subjected to 45 min of ischaemia and 1 week of reperfusion to establish a myocardial I/R injury model. A miR-146a mimic (0.5 mg/kg) was administered intravenously at the beginning of the ischaemia process. Neonatal rat cardiomyocytes were also subjected to hypoxia/reperfusion (H/R). Cells were treated with the miR-146a mimic or antagonist. As a result, the miR-146a mimic attenuated H/R-induced cardiomyocyte injury, as evidenced by increased cell viability and reduced lactate dehydrogenase (LDH) levels. In addition, the miR-146a mimic inhibited oxidative stress in cells suffering from H/R injury. Moreover, the miR-146a antagonist exerted adverse effects in vitro. In mice with myocardial I/R injury, the miR-146a mimic preserved cardiac function and reduced the infarction area and fibrosis. Moreover, the miR-146a mimic decreased the inflammatory response and reactive oxygen species (ROS) accumulation in mouse hearts. Mechanistically, we found that miR-146a directly regulated the transcription of NOX4, which subsequently affected P38 signalling in cardiomyocytes. When we knocked down NOX4, the effects of the miR-146a antagonist in worsening the cell condition were counteracted in in vitro experiments. Taken together, the results suggest that miR-146a protects against myocardial ischaemia reperfusion injury by inhibiting NOX4 signalling. The miR-146a mimic may become a potential therapeutic approach for patients with myocardial ischaemia reperfusion.
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