Project 171747
Transformation of normal to abnormal myocardium by diabetes mellitus: role of Rac1-mediated calpain activation
Transformation of normal to abnormal myocardium by diabetes mellitus: role of Rac1-mediated calpain activation
Project Information
| Study Type: | Unclear |
| Research Theme: | Biomedical |
Institution & Funding
| Principal Investigator(s): | Peng, Tianqing |
| Co-Investigator(s): | Arany, Edith J |
| Institution: | London Health Sciences Centre Res. Inc. (Ont.) |
| CIHR Institute: | Circulatory and Respiratory Health |
| Program: | |
| Peer Review Committee: | Cardiovascular System - B: Heart and Circulation |
| Competition Year: | 2008 |
| Term: | 3 yrs 0 mth |
Abstract Summary
Diabetes is a disease. Patients' body with this disease can not properly utilize sugar (glucose). Thus, there is an increased concentration of sugar in blood of diabetic patients. There are two main types of this disease: type-1 and type-2 diabetes. The prevalence of diabetes is growing rapidly. Globally, the number of adults affected with diabetes is estimated to increase from 135 million in 1995 to 300 million by 2025. Patients with diabetes are at increased risk for heart and blood vessel diseases. Heart and vessel diseases are the leading cause of diabetes-related death. Diabetes can directly damage heart and cause the heart not working properly, a condition called diabetic cardiomyopathy. Diabetic cardiomyopathy occurs independently of other heart disorders such as heart vessel disease and high blood pressure. However, how diabetes causes diabetic cardiomyopathy remains not fully understood. Excessive oxidant products have been linked to the onset of diabetic cardiomyopathy. Recent studies have found that damage caused by oxidant products plays a critical role in diabetic cardiomyopathy. Oxidant products are generated by different sources, among which an enzyme called NADPH oxidase has been suggested as a main source in heart muscle cells. A protein called Rac1 is an important subunit of this enzyme and is required for this enzyme's activation. However, the role of Rac1 in diabetic cardiomyopathy has not been fully elucidated. Thus, the present study is aimed to understand if Rac1 plays a role in development of diabetic cardiomyopathy and how Rac1 causes this heart disorder. The results from this study will help to design the treatment methods for diabetic cardiomyopathy.
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