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Rats were maintained for a further 8 weeks. Rats (<jats:italic>n<\/jats:italic> = 36) were randomized into four groups: Sham+Sham, Sham+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> STN<\/jats:styled-content>x+Sham and <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. Increased renal tubulointerstitial fibrosis (<jats:italic>P<\/jats:italic> &lt; 0.01) and kidney injury molecule\u20101 expression (<jats:italic>P<\/jats:italic> &lt; 0.01) was observed in <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> compared to <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+Sham animals, while there were no further reductions in renal function. Heart weight was increased in <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> compared to <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+Sham or Sham+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> animals (<jats:italic>P<\/jats:italic> &lt; 0.05), despite no difference in blood pressure. <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> rats demonstrated greater cardiomyocyte cross\u2010sectional area and increased cardiac interstitial fibrosis compared to either <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x+Sham (<jats:italic>P<\/jats:italic> &lt; 0.01) or Sham+<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> (<jats:italic>P<\/jats:italic> &lt; 0.01) animals which was accompanied by an increase in diastolic dysfunction. These changes were associated with increases in <jats:styled-content style=\"fixed-case\">ANP<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> cTGF<\/jats:styled-content> and collagen I gene expression and phospho\u2010p38 <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> and phospho\u2010p44\/42 <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> protein expression in the left ventricle. Addition of <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> accelerated <jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>x\u2010induced structural damage but failed to significantly exacerbate renal dysfunction. These findings highlight the bidirectional response in this model known to occur in cardiorenal syndrome (<jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>) and provide a useful model for examining potential therapies for <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/jcmm.13349","type":"journal-article","created":{"date-parts":[[2017,10,10]],"date-time":"2017-10-10T08:18:40Z","timestamp":1507623520000},"page":"628-645","source":"Crossref","is-referenced-by-count":9,"title":["Chronic kidney disease with comorbid cardiac dysfunction exacerbates cardiac and renal damage"],"prefix":"10.1111","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3871-9320","authenticated-orcid":false,"given":"Shan","family":"Liu","sequence":"first","affiliation":[{"name":"School of Medicine South China University of Technology China"},{"name":"Centre of Cardiovascular Research and Education in Therapeutics Department of Epidemiology and Preventive Medicine Monash University Melbourne Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bing H.","family":"Wang","sequence":"additional","affiliation":[{"name":"Centre of Cardiovascular Research and Education in Therapeutics Department of Epidemiology and Preventive Medicine Monash University Melbourne Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darren J.","family":"Kelly","sequence":"additional","affiliation":[{"name":"Department of Medicine St. Vincent's Hospital University of Melbourne Melbourne Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Henry","family":"Krum","sequence":"additional","affiliation":[{"name":"Centre of Cardiovascular Research and Education in Therapeutics Department of Epidemiology and Preventive Medicine Monash University Melbourne Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew 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