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Tissue endomyocardial biopsy samples divided into three groups according to LVEF ((I) 45\u201350%,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">10<\/mml:mn><\/mml:math>; (II) 30\u201340%,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">15<\/mml:mn><\/mml:math>; (III) &lt;30%,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">15<\/mml:mn><\/mml:math>; and control (donor hearts, &gt;60%,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">6<\/mml:mn><\/mml:math>)) were investigated. The PPAR<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\"><mml:mrow><mml:mi>\u03b1<\/mml:mi><\/mml:mrow><\/mml:math>mRNA expression in the failing hearts was low in Group (I), high in Group (II), and comparable to that of the control in Group (III). There were analogous changes in the expression of FAT\/CD36 and CPT-1 mRNA in contrast to continuous overexpression of GLUT-4 mRNA and significant increase of PDK-4 mRNA in Group (II). In addition, significant structural changes of cardiomyocytes with glycogen accumulation were accompanied by increased expression of PPAR<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\"><mml:mrow><mml:mi>\u03b1<\/mml:mi><\/mml:mrow><\/mml:math>. For the entire study population with HF levels of FAT\/CD36 mRNA showed a strong tendency of negative correlation with LVEF. In conclusion, PPAR<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\"><mml:mrow><mml:mi>\u03b1<\/mml:mi><\/mml:mrow><\/mml:math>elevated levels may be a direct cause of adverse remodeling, both metabolic and structural. Thus, there is limited time window for therapy modulating cardiac metabolism and protecting cardiomyocyte structure in failing heart.<\/jats:p>","DOI":"10.1155\/2016\/7508026","type":"journal-article","created":{"date-parts":[[2016,2,15]],"date-time":"2016-02-15T21:01:15Z","timestamp":1455570075000},"page":"1-12","source":"Crossref","is-referenced-by-count":10,"title":["The Correlation of PPAR<i>\u03b1<\/i>Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression"],"prefix":"10.1155","volume":"2016","author":[{"given":"E.","family":"Czarnowska","sequence":"first","affiliation":[{"name":"Department of Pathology, The Children\u2019s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Domal-Kwiatkowska","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Silesia in Katowice, Jedno\u015bci Street 8, 41-200 Sosnowiec, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"Reichman-Warmusz","sequence":"additional","affiliation":[{"name":"Department of Histology, School of Medicine with the Division of Dentistry, Medical University of Silesia in Katowice, Jordana Street 19, 41-808 Zabrze, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. B.","family":"Bierla","sequence":"additional","affiliation":[{"name":"Department of Pathology, The Children\u2019s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Sowinska","sequence":"additional","affiliation":[{"name":"Department of Pathology, The Children\u2019s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Ratajska","sequence":"additional","affiliation":[{"name":"Department of Pathology, The Medical University of Warsaw, T. 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