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Although a large amount of evidence indicates that activation of \u03b17 nicotinic acetylcholine receptor (\u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>hR) causes an anti\u2010inflammatory effect, the role of \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>hR in cardiac remodelling and the underlying mechanism have not been established. To investigate the effect of the specific \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>hR agonist, <jats:styled-content style=\"fixed-case\">PNU<\/jats:styled-content>282987, on cardiac remodelling induced by isoproterenol (<jats:styled-content style=\"fixed-case\">ISO<\/jats:styled-content> 60\u00a0mg\/kg per day) in mice, the cardiomyocyte cross\u2010sectional area (<jats:styled-content style=\"fixed-case\">CSA<\/jats:styled-content>) and collagen volume fraction were evaluated by hematoxylin and eosin (<jats:styled-content style=\"fixed-case\">HE<\/jats:styled-content>) and Masson staining, respectively. Cardiac function and ventricular wall thickness were measured by echocardiography. The protein expressions of collagen I, matrix metalloproteinase 9 (<jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20109), transforming growth factor \u03b21 (<jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b21), and Smad3 were analyzed by Western blot. <jats:styled-content style=\"fixed-case\">ISO<\/jats:styled-content>\u2010induced cardiac hypertrophy, characterized by an increase in the heart weight\/body weight ratio, <jats:styled-content style=\"fixed-case\">CSA<\/jats:styled-content> and ventricular wall thickness. Moreover, cardiac fibrosis indices, such as collagen volume fraction, <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20109 and collagen I protein expression, were also increased by <jats:styled-content style=\"fixed-case\">ISO<\/jats:styled-content>. PNU282987 not only attenuated cardiac hypertrophy but also decreased the cardiac fibrosis induced by <jats:styled-content style=\"fixed-case\">ISO<\/jats:styled-content>. Furthermore, PNU282987 suppressed <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b21 protein expression and the phosphorylation of Smad3 induced by <jats:styled-content style=\"fixed-case\">ISO<\/jats:styled-content>. In conclusion, PNU282987 ameliorated the cardiac remodelling induced by <jats:styled-content style=\"fixed-case\">ISO<\/jats:styled-content>, which may be related to the <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b21\/Smad3 pathway. These data imply that the \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>hR may represent a novel therapeutic target for cardiac remodelling in many cardiovascular diseases.<\/jats:p>","DOI":"10.1111\/1440-1681.12819","type":"journal-article","created":{"date-parts":[[2017,7,21]],"date-time":"2017-07-21T16:27:43Z","timestamp":1500654463000},"page":"1192-1200","source":"Crossref","is-referenced-by-count":13,"title":["Specific \u03b17 nicotinic acetylcholine receptor agonist ameliorates isoproterenol\u2010induced cardiac remodelling in mice through <scp>TGF<\/scp>\u2010\u03b21\/Smad3 pathway"],"prefix":"10.1111","volume":"44","author":[{"given":"Yong\u2010Hua","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Paediatrics the First Affiliated Hospital of Xi'an Jiaotong University  Xi'an China"},{"name":"Department of Pharmacology Xi'an Jiaotong University Health Science Centre  Xi'an 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