The role of PPARδ in the diabetic cardiomyopathy

Previous studies showed that reactive oxygen species (ROS) is critically involved in the pathogenesis of diabetic cardiomyopathy. In recent, the cardiac peroxisome proliferator‐activated receptor (PPAR)‐δ deficiency is respected an important marker in the cardiomyopathy and cardiac dysfunction, whil...

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Bibliographic Details
Published in:The FASEB journal 2006-03, Vol.20 (5), p.LB106-LB106
Main Authors: Yu, Bu‐Chin, Cheng, Juei‐Tang
Format: Article
Language:English
Online Access:Get full text
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Summary:Previous studies showed that reactive oxygen species (ROS) is critically involved in the pathogenesis of diabetic cardiomyopathy. In recent, the cardiac peroxisome proliferator‐activated receptor (PPAR)‐δ deficiency is respected an important marker in the cardiomyopathy and cardiac dysfunction, while the PPARδ expression in diabetic cardiomyopathy is not clear. Therefore, the aim of this study is going to investigate the role of PPARδ in the pathogenesis of diabetic cardiomyopathy. We examined the changes in streptozotocin‐induced diabetic rats 12 weeks after induction of diabetes. These diabetic animals showed cardiac hypertrophy and cardiac dysfunction. Also, the gene expression of cardiac PPARδ was decreased. In order to know the effect of hyperglycemia on PPARδ, the H9c2 cell (rat cardiomyocytes) was employed in advance. The PPARδ expression was reduced in time and dose related manner by glucose. The decline of PPARδ expression was prevented by the inhibitors of ROS generation. Thus, it can be concluded that hyperglycemia‐induced ROS is responsible for diabetic cardiomyopathy through the decrease of PPARδ expression.
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.20.5.LB106-c