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PARP mediates structural alterations in diabetic cardiomyopathy.
Jane Chiu1, Hana Farhangkhoee, Bing Ying Xu
1Department of Pathology, 4033 Dental Sciences Building, University of Western Ontario, London, Ontario, Canada.
Journal of Molecular and Cellular Cardiology
|July 29, 2008
Summary
Diabetic cardiomyopathy involves heart structural changes. This study reveals poly (ADP-ribose) polymerase (PARP) drives these changes via oxidative stress and p300, offering new therapeutic targets.
Area of Science:
- Cardiovascular Biology
- Metabolic Diseases
- Molecular Medicine
Background:
- Diabetic cardiomyopathy is a significant complication of diabetes mellitus.
- Oxidative stress and hyperglycemia are implicated in its pathogenesis.
- Poly (ADP-ribose) polymerase (PARP) activation is linked to cellular damage and gene expression.
Purpose of the Study:
- To investigate the role of PARP in diabetes-induced cardiac structural alterations.
- To elucidate the mechanisms linking PARP, oxidative stress, and heart damage in diabetes.
- To identify potential therapeutic targets for diabetic cardiomyopathy.
Main Methods:
- Utilized PARP-1 knockout mice and streptozotocin-induced diabetic rats.
- Administered PARP inhibitor 3-aminobenzamide (ABA) in vivo.
- Verified findings in vitro using neonatal cardiomyocytes and endothelial cells.
Main Results:
- Hyperglycemia increased extracellular matrix proteins, p300 levels, cardiomyocyte hypertrophy, and oxidative stress.
- These diabetes-induced changes were prevented in PARP-deficient mice and ABA-treated rats.
- Evidence suggests histone deacetylases influence these PARP-mediated pathways.
Conclusions:
- A novel PARP-dependent, p300-associated pathway mediates structural alterations in the diabetic heart.
- Targeting PARP may offer a therapeutic strategy for diabetic cardiomyopathy.
- This pathway involves oxidative stress and epigenetic modifications.
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