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Myocardial hypertrophy is a common symptom in numerous cardiovascular diseases. In the current study, we attempted to demonstrate the role of miR\u2010143\u20103p in the development of myocardial hypertrophy by focusing on its association with inflammation. Myocardial hypertrophy was induced by transverse aortic constriction (TAC) method in vivo and by H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> administration in vitro. The expression status of miR\u2010143\u20103p and downstream effectors were detected in animal heart tissues and H9c2 cells. Furthermore, the effect of miR\u2010143\u20103p inhibition on H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010induced changes in ERK5\/PPAR\u03b4\/NF\u2010\u03baB axis was assessed. TAC induced oxidative stress and inflammation in rat heart tissues, which was associated with the increased expressions of miR\u2010143\u20103p and p\u2010ERK5. However, the up\u2010regulated expression of miR\u2010143\u20103p had no effect on the expression of ERK5, which was a direct target of miR\u2010143\u20103p. The results of in vitro assays showed that H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> administration increased the levels of miR\u2010143\u20103p and p\u2010EKR5 and induced the activation of NF\u2010\u03baB pathway. After the inhibition of miR\u2010143\u20103p, the activation of EKR5 and NF\u2010\u03baB pathway was suppressed, whereas the expression of PPAR\u03b4 was up\u2010regulated. The current study demonstrated that miR\u2010143\u20103p is crucial to the initiation of inflammatory response induced by myocardial hypertrophy. The activation of ERK5 following miR\u2010143\u20103p up\u2010regulation appears to be a complementary response to induce the subsequent anti\u2010inflammatory signaling transduction, which needed further exploration.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbin.11053","type":"journal-article","created":{"date-parts":[[2018,9,11]],"date-time":"2018-09-11T16:21:22Z","timestamp":1536682882000},"page":"1584-1593","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Inhibition of microRNA\u2010143\u20103p attenuates myocardial hypertrophy by inhibiting inflammatory response"],"prefix":"10.1002","volume":"42","author":[{"given":"Bo","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Cardiology Jilin Provincial Key Laboratory for Genetic Diagnosis of Cardiovascular Disease China\u2010Japan Union Hospital of Jilin University 126 Xiantai Avenue Changchun 130033 People's Republic of 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