Alcohol is a major public health concern in the United States due to the various well-documented pathological conditions associated with its use and abuse. Alcohol-induced heart disease is responsible for significant amount of morbidity and mortality in alcoholics, however, the understanding of many of the underlying molecular mechanisms remains elusive. The goal of this study is to test the hypotheses that 1) uncoupling protein-2 (UCP2) expression and activity has direct consequences which contribute to decreased myocardial contractility and the development of heart failure in alcoholic cardiomyopathy (ACM), 2) oxidative damage due to generation of excess reactive oxygen species (ROS) contributes to disease onset and progression, and UCP2 expression is induced in an effort to dampen ROS generation and to prevent further oxidative damage, and 3) this adaptive change leading to UCP2 expression leads to decreased ATP production, thus hindering various ATP-dependent cellular processes and ultimately contributing to compromised myocardial function and heart failure.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Individual Predoctoral NRSA for M.D./Ph.D. Fellowships (ADAMHA) (F30)
Project #
1F30AA015004-01
Application #
6791746
Study Section
Special Emphasis Panel (ZAA1-EE (01))
Program Officer
Brown, Ricardo A
Project Start
2004-07-01
Project End
2008-06-30
Budget Start
2004-07-01
Budget End
2005-06-30
Support Year
1
Fiscal Year
2004
Total Cost
$29,157
Indirect Cost
Name
University of Medicine & Dentistry of NJ
Department
Pharmacology
Type
Schools of Medicine
DUNS #
623946217
City
Newark
State
NJ
Country
United States
Zip Code
07107
Turner, Jay D; Gaspers, Lawrence D; Wang, Guoqiang et al. (2010) Uncoupling protein-2 modulates myocardial excitation-contraction coupling. Circ Res 106:730-8