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The aim of this study was to test the hypothesis that miR\u2010200c plays an important role in the progression of CH by targeting myosin light chain kinase (MLCK\/MYLK).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>Cardiac 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\u2010time PCR (qRT\u2010PCR) and Western blotting were used to measure mRNA and protein levels respectively. The present results showed that miR\u2010200c expression was increased in response to CH both in vivo and in vitro. The down\u2010regulation of miRNA\u2010200c by a specific inhibitor markedly ameliorated CH resulting from AngII treatment, and the mRNA levels of atrial natriuretic peptide, brain natriuretic peptide and \u03b2\u2010myosin heavy chain were simultaneously decreased. Notably, minimal apoptosis and ROS accumulation were identified in AngII\u2010induced hypertrophic cardiomyocytes. Conversely, the up\u2010regulation of miR\u2010200c using specific mimics reversed these effects. Mechanistic investigations demonstrated that the MLCK gene is a direct target of miR\u2010200c; an increase in miR\u2010200c levels led to a decrease in the expression of MLCK and its downstream effector, p\u2010MLC2, while miR\u2010200c inhibition increased the expression of these proteins. Furthermore, inhibiting MLCK impaired the anti\u2010hypertrophic effects contributions produced by the knockdown of miR\u2010200c.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our studies suggest that miR\u2010200c may serve as a potential therapeutic target that could delay hypertrophy. We have also uncovered a relationship between miR\u2010200c and MLCK, identifying MLCK as a direct mediator of miR\u2010200c.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jcmm.14135","type":"journal-article","created":{"date-parts":[[2019,1,25]],"date-time":"2019-01-25T08:20:48Z","timestamp":1548404448000},"page":"2505-2516","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Down\u2010regulation of miR\u2010200c attenuates AngII\u2010induced cardiac hypertrophy via targeting the MLCK\u2010mediated pathway"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2984-5317","authenticated-orcid":false,"given":"Shan","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology Wuhan 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