The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression

This study aimed to define relationship between PPARα expression and metabolic-structural characteristics during HF progression in hearts with DCM phenotype. Tissue endomyocardial biopsy samples divided into three groups according to LVEF ((I) 45–50%, n=10; (II) 30–40%, n=15; (III) <30%, n=15; an...

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Main Authors: E. Czarnowska, D. Domal-Kwiatkowska, E. Reichman-Warmusz, J. B. Bierla, A. Sowinska, A. Ratajska, K. Goral-Radziszewska, R. Wojnicz
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2016/7508026
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author E. Czarnowska
D. Domal-Kwiatkowska
E. Reichman-Warmusz
J. B. Bierla
A. Sowinska
A. Ratajska
K. Goral-Radziszewska
R. Wojnicz
author_facet E. Czarnowska
D. Domal-Kwiatkowska
E. Reichman-Warmusz
J. B. Bierla
A. Sowinska
A. Ratajska
K. Goral-Radziszewska
R. Wojnicz
author_sort E. Czarnowska
collection DOAJ
description This study aimed to define relationship between PPARα expression and metabolic-structural characteristics during HF progression in hearts with DCM phenotype. Tissue endomyocardial biopsy samples divided into three groups according to LVEF ((I) 45–50%, n=10; (II) 30–40%, n=15; (III) <30%, n=15; and control (donor hearts, >60%, n=6)) were investigated. The PPARα 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 PPARα. For the entire study population with HF levels of FAT/CD36 mRNA showed a strong tendency of negative correlation with LVEF. In conclusion, PPARα 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.
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spelling doaj-art-206b21ac3b0847a78ba58fdb6fc3c9072025-02-03T01:29:55ZengWileyPPAR Research1687-47571687-47652016-01-01201610.1155/2016/75080267508026The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure ProgressionE. Czarnowska0D. Domal-Kwiatkowska1E. Reichman-Warmusz2J. B. Bierla3A. Sowinska4A. Ratajska5K. Goral-Radziszewska6R. Wojnicz7Department of Pathology, The Children’s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, PolandDepartment of Biochemistry, Medical University of Silesia in Katowice, Jedności Street 8, 41-200 Sosnowiec, PolandDepartment of Histology, School of Medicine with the Division of Dentistry, Medical University of Silesia in Katowice, Jordana Street 19, 41-808 Zabrze, PolandDepartment of Pathology, The Children’s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, PolandDepartment of Pathology, The Children’s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, PolandDepartment of Pathology, The Medical University of Warsaw, T. Chałubińskiego Street 5, 02-004 Warsaw, PolandDepartment of Genetics and Animal Breeding, Faculty of Animal Science, Warsaw University of Life Sciences-SGGW, Ciszewskiego Street 8, 02-786 Warsaw, PolandDepartment of Histology and Embryology, Medical University of Silesia in Katowice, Jordana Street 19, 41-808 Zabrze, PolandThis study aimed to define relationship between PPARα expression and metabolic-structural characteristics during HF progression in hearts with DCM phenotype. Tissue endomyocardial biopsy samples divided into three groups according to LVEF ((I) 45–50%, n=10; (II) 30–40%, n=15; (III) <30%, n=15; and control (donor hearts, >60%, n=6)) were investigated. The PPARα 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 PPARα. For the entire study population with HF levels of FAT/CD36 mRNA showed a strong tendency of negative correlation with LVEF. In conclusion, PPARα 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.http://dx.doi.org/10.1155/2016/7508026
spellingShingle E. Czarnowska
D. Domal-Kwiatkowska
E. Reichman-Warmusz
J. B. Bierla
A. Sowinska
A. Ratajska
K. Goral-Radziszewska
R. Wojnicz
The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression
PPAR Research
title The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression
title_full The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression
title_fullStr The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression
title_full_unstemmed The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression
title_short The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression
title_sort correlation of pparα activity and cardiomyocyte metabolism and structure in idiopathic dilated cardiomyopathy during heart failure progression
url http://dx.doi.org/10.1155/2016/7508026
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