ArticleCellular & molecular biology letters2017
MicroRNA-210 induces endothelial cell apoptosis by directly targeting PDK1 in the setting of atherosclerosis.
Article in Cellular & molecular biology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 96 citations in OpenAlex.
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- Bioengineered Cellular and Acellular Therapies for Ischemic Heart Disease in Clinically Relevant Models.Bioengineering (Basel, Switzerland) · 2026Review
- Metabolism-related gene PDK1 regulates myocardial cell remodeling and its mechanism.Stem cell research & therapy · 2025Article
- Exosomes: bridge metabolic regulation in cardiac repair.npj biomedical innovations · 2025Review
- Suppression of breast cancer metastatic behavior by microRNAs targeting EMT transcription factors. A relevant participation of miR-196a-5p and miR-22-3p in ZEB1 expression.Breast cancer research and treatment · 2025Article
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- Connecting the Dots: How MicroRNAs Link Asthma and Atherosclerosis.International journal of molecular sciences · 2025Review
- Cellular Phenotypic Transformation During Atherosclerosis: The Potential Role of miRNAs as Biomarkers.International journal of molecular sciences · 2025Review
- Cardioepigenetics in action: aerobic exercise-induced modulation of miRNAs, lncRNAs, and chromatin remodeling in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Biogenerated Oxygen-Related Environmental Stressed Apoptotic Vesicle Targets Endothelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- MiR-130a-3p inhibits endothelial inflammation by regulating the expression of MAPK8 in endothelial cells.Heliyon · 2024Article
- Decoding the secrets of longevity: unraveling nutraceutical and miRNA-Mediated aging pathways and therapeutic strategies.Frontiers in aging · 2024Review
- PCSK9i promoting the transformation of AS plaques into a stable plaque by targeting the miR-186-5p/Wipf2 and miR-375-3p/Pdk1/Yap1 in ApoE-/- mice.Frontiers in medicine · 2024Article
- The Mechanisms of miRNAs on Target Regulation and their Recent Advances in Atherosclerosis.Current medicinal chemistry · 2024Review
- MiR-15b-5p and PCSK9 inhibition reduces lipopolysaccharide-induced endothelial dysfunction by targeting SIRT4.Cellular & molecular biology letters · 2023Article
- Silencing METTL3 Stabilizes Atherosclerotic Plaques by Regulating the Phenotypic Transformation of Vascular Smooth Muscle Cells via the miR-375-3p/PDK1 Axis.Cardiovascular drugs and therapy · 2023Article
- Pathogenic role of microRNAs in atherosclerotic ischemic stroke: Implications for diagnosis and therapy.Genes & diseases · 2022Review
- Therapeutic Potential of Stem Cell-Derived Extracellular Vesicles on Atherosclerosis-Induced Vascular Dysfunction and Its Key Molecular Players.Frontiers in cell and developmental biology · 2022Article
- LINC00460 Stimulates the Proliferation of Vascular Endothelial Cells by Downregulating miRNA-24-3p.Disease markers · 2022Article
- miR-210 Regulates Apoptotic Cell Death during Cellular Hypoxia and Reoxygenation in a Diametrically Opposite Manner.Biomedicines · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherosclerosis is a chronically inflammatory disease and one of the leading causes of deaths worldwide. Endothelial cell apoptosis plays a crucial role in its development. Several microRNAs (miRNAs) are reportedly involved in atherosclerotic plaque formation, including miRNA-210 (miR-210). However, the underlying mechanism of its role in endothelial cell apoptosis during atherosclerosis is still largely unknown.
methodsA mouse model with atherosclerosis induced by a high-fat diet (HFD) was built in ApoE (-/-) mice. The levels of endothelial cell apoptosis were determined via flow cytometry. The expressions of miR-210 and PDK1 in purified CD31+ endothelial cells from mouse aorta were measured via RT-qPCR and western blot. Binding between miR-210 and the 3'-untranslated region (UTR) of PDK1 mRNA was predicted using bioinformatics analyses and confirmed with a dual luciferase reporter assay. The effects of miR-210 were further analyzed in an in vitro model using human aortic endothelial cells (HAECs) treated with oxidized low-density lipoprotein (ox-LDL).
resultsWe found that the HFD mice developed atherosclerosis in 12 weeks and had a significantly higher percentage of endothelial cell apoptosis. The upregulated level of miR-210 in the HFD mice and HAECs inversely correlated with the level of PDK1. Inhibiting miR-210 expression significantly reduced HAEC apoptosis, as evidenced by the results of the MTT and flow cytometry experiments. Further analysis identified PDK1 as the target of miR-210 and showed that PDK1 overexpression reversed the pro-apoptotic effect of miR-210 through mediation of the P13K/Akt/mTOR pathways.
conclusionOur study suggests a novel role for miR-210 in the progression of atherosclerosis through the regulation of endothelial apoptosis. This indicates that miR-210 might have potential in treatment of atherosclerosis.
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