ArticleJournal of cellular and molecular medicine2019
Down-regulation of miR-200c attenuates AngII-induced cardiac hypertrophy via targeting the MLCK-mediated pathway.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The Network of Exosomes miRNA and p-MLC2 Regulatory Pathway Induced Pathological Cardiac Hypertrophy in Vasn Deficient Mice.Journal of cellular and molecular medicine · 2025Article
- Divergent Cardiovascular Adaptations and Gene Regulation in High-Elevation Natives and Recent Colonizers of the Qinghai-Tibetan Plateau.Molecular biology and evolution · 2025Article
- Correction to Down-regulation of miR-200c attenuates AngII-induced cardiac hypertrophy via targeting the MLCK-mediated pathway.Journal of cellular and molecular medicine · 2023Article
- lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.Bioengineered · 2022Article
- MicroRNA miR-27a-3p accelerates cardiac hypertrophy by targeting neuro-oncological ventral antigen 1.Bioengineered · 2022Article
- Loss of cardiac myosin light chain kinase contributes to contractile dysfunction in right ventricular pressure overload.Physiological reports · 2022Article
- Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice.Journal of cellular and molecular medicine · 2022Article
- Myosin Light Chain Kinase Modulates to Improve Myocardial Hypoxia/Reoxygenation Injury.Journal of healthcare engineering · 2022Article
- TFEC contributes to cardiac hypertrophy by inhibiting AMPK/mTOR signaling.Experimental and therapeutic medicine · 2021Article
- Amniotic fluid microRNA profiles in twin-twin transfusion syndrome with and without severe recipient cardiomyopathy.American journal of obstetrics and gynecology · 2021Article
- Piperine protects against myocardial ischemia/reperfusion injury by activating the PI3K/AKT signaling pathway.Experimental and therapeutic medicine · 2021Article
- Myocardial Infarction: The Protective Role of MiRNAs in Myocardium Pathology.Frontiers in cardiovascular medicine · 2021Review
- Up-regulation of miR-195 contributes to cardiac hypertrophy-induced arrhythmia by targeting calcium and potassium channels.Journal of cellular and molecular medicine · 2020Article
- MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Long Noncoding RNA FTX Reduces Hypertrophy of Neonatal Mouse Cardiac Myocytes and Regulates the PTEN/PI3K/Akt Signaling Pathway by Sponging MicroRNA-22.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- MD-1 Deficiency Accelerates Myocardial Inflammation and Apoptosis in Doxorubicin-Induced Cardiotoxicity by Activating the TLR4/MAPKs/Nuclear Factor kappa B (NF-κB) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- MicroRNAs in Cardiac Hypertrophy.International journal of molecular sciences · 2019Review
- Down-regulation of miR-200c attenuates AngII-induced cardiac hypertrophy via targeting the MLCK-mediated pathway.Journal of cellular and molecular medicine · 2019Article
- The Oxidative Stress-Induced miR-200c Is Upregulated in Psoriasis and Correlates with Disease Severity and Determinants of Cardiovascular Risk.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs (miRNAs) have been shown to commonly contribute to cardiac hypertrophy (CH). The aim of this study was to test the hypothesis that miR-200c plays an important role in the progression of CH by targeting myosin light chain kinase (MLCK/MYLK). METHODS AND
resultsCardiac hypertrophy was induced by aortic banding (AB) in rats. Cellular hypertrophy in neonatal rat cardiomyocytes (NCMs) was induced by AngII treatment. Echocardiography, histology and molecular measurements were used to assess the results of the experiments. The levels of apoptosis and reactive oxygen species (ROS) were also measured. Quantitative real-time PCR (qRT-PCR) and Western blotting were used to measure mRNA and protein levels respectively. The present results showed that miR-200c expression was increased in response to CH both in vivo and in vitro. The down-regulation of miRNA-200c by a specific inhibitor markedly ameliorated CH resulting from AngII treatment, and the mRNA levels of atrial natriuretic peptide, brain natriuretic peptide and β-myosin heavy chain were simultaneously decreased. Notably, minimal apoptosis and ROS accumulation were identified in AngII-induced hypertrophic cardiomyocytes. Conversely, the up-regulation of miR-200c using specific mimics reversed these effects. Mechanistic investigations demonstrated that the MLCK gene is a direct target of miR-200c; an increase in miR-200c levels led to a decrease in the expression of MLCK and its downstream effector, p-MLC2, while miR-200c inhibition increased the expression of these proteins. Furthermore, inhibiting MLCK impaired the anti-hypertrophic effects contributions produced by the knockdown of miR-200c.
conclusionOur studies suggest that miR-200c may serve as a potential therapeutic target that could delay hypertrophy. We have also uncovered a relationship between miR-200c and MLCK, identifying MLCK as a direct mediator of miR-200c.
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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.