ArticleMolecular and cellular biochemistry2016
CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Impact ofJournal of cardiovascular development and disease · 2026Review
- Global Perspectives on Coronary Artery Disease: The Emerging Role of miRNAs.Current atherosclerosis reports · 2025Review
- Cyclin-dependent protein kinases and cell cycle regulation in biology and disease.Signal transduction and targeted therapy · 2025Review
- Multiple Copies of microRNA Binding Sites in Long 3'UTR Variants Regulate Axonal Translation.Cells · 2023Article
- Epigenome-wide DNA methylation profiling in comparison between pathological and physiological hypertrophy of human cardiomyocytes.Frontiers in genetics · 2023Article
- Suppression of the Inhibitory Effect of circ_0036176-Translated Myo9a-208 on Cardiac Fibroblast Proliferation by miR-218-5p.Journal of cardiovascular translational research · 2022Article
- LncRNA ROR modulates myocardial ischemia-reperfusion injury mediated by the miR-185-5p/CDK6 axis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Diverging targets mediate the pathological roleof miR-199a-5p and miR-199a-3p by promoting cardiac hypertrophy and fibrosis.Molecular therapy. Nucleic acids · 2021Article
- Dickkopf 3: a Novel Target Gene of miR-25-3p in Promoting Fibrosis-Related Gene Expression in Myocardial Fibrosis.Journal of cardiovascular translational research · 2021Article
- The Impact of microRNAs in Renin-Angiotensin-System-Induced Cardiac Remodelling.International journal of molecular sciences · 2021Review
- Myocardial Infarction: The Protective Role of MiRNAs in Myocardium Pathology.Frontiers in cardiovascular medicine · 2021Review
- Circulating miR-4763-3p Is a Novel Potential Biomarker Candidate for Human Adult Fulminant Myocarditis.Molecular therapy. Methods & clinical development · 2020Article
- Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p binding to Gata4.Cardiovascular research · 2020Article
- [Overexpression of miR-130a-3p attenuates cardiomyocyte hypertrophy].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020Article
- [CircRNA_005647 inhibits expressions of fibrosis-related genes in mouse cardiac fibroblastsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- MicroRNAs in Cardiac Hypertrophy.International journal of molecular sciences · 2019Review
- Identification of microRNAs and genes as biomarkers of atrial fibrillation using a bioinformatics approach.The Journal of international medical research · 2019Article
- MicroRNAs in Cardiac Diseases.Cells · 2019Review
- Adaptation of Human iPSC-Derived Cardiomyocytes to Tyrosine Kinase Inhibitors Reduces Acute Cardiotoxicity via Metabolic Reprogramming.Cell systems · 2019Article
- Premature MicroRNA-1 Expression Causes Hypoplasia of the Cardiac Ventricular Conduction System.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-1 (miR-1) is approved involved in cardiac hypertrophy, but the underlying molecular mechanisms of miR-1 in cardiac hypertrophy are not well elucidated. The present study aimed to investigate the potential role of miR-1 in modulating CDKs-Rb pathway during cardiomyocyte hypertrophy. A rat model of hypertrophy was established with abdominal aortic constriction, and a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocytes (NRVCs). We demonstrated that miR-1 expression was markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes. Dual luciferase reporter assays revealed that miR-1 interacted with the 3'UTR of CDK6, and miR-1 was verified to inhibit CDK6 expression at the posttranscriptional level. CDK6 protein expression was observed increased in hypertrophic myocardium and hypertrophic cardiomyocytes. Morover, miR-1 mimic, in parallel to CDK6 siRNA, could inhibit PE-induced hypertrophy of NRVCs, with decreases in cell size, newly transcribed RNA, expressions of ANF and β-MHC, and the phosphorylated pRb. Taken together, our results reveal that derepression of CDK6 and activation of Rb pathway contributes to the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy.
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