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The role of inflammatory responses in Alcoholic Cardiomyopathy
Author(s) -
Walker Robin K,
Haddad Georges E
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1128.9
Subject(s) - alcoholic cardiomyopathy , oxidative stress , medicine , cardiomyopathy , protein kinase b , alcohol , ethanol metabolism , heart disease , heart failure , cardiology , endocrinology , signal transduction , biochemistry , metabolism , biology
Cardiovascular disease is among the major causes for increased morbidity and mortality rates. High alcohol consumption may lead to cardiomyopathy, cardiac arrhythmias, and a suite of other disorders. Previous studies in our lab have linked the AKT/PI3K pathway to cardiac hypertrophy. Alcohol consumption induces oxidative stress and increases the risk of heart disease, and several other complications involving metabolic disturbances and organ damage. Clinical features of the consequences of prolonged and excessive ethanol consumption encompass defects in myocardial contractility and derangement of cellular architecture. Oxidative stress has been reported to be the major contributor for these alcohol induced pathologies. In the present study, our aim is to investigate the effects of chronic alcohol treatments on expression of NRF2, a core regulator of antioxidant machinery on oxidative stress markers of alcohol induced cardiomyopathy. Our preliminary results in chronic alcoholic rats show that with increasing concentrations of alcohol from low (0.023% Ethanol) to High (0.461% Ethanol) we increase NRF2 and SOD‐3 gene expression. Our data suggest that NRF2 may act as a molecular switch to control the oxidative balance during chronic alcohol consumption in the heart. We will use this data to continue to examine the link between NRF2 signaling and the AKT/PI3K pathway in alcohol‐induced cardiomyopathy. This work was supported in part by grants NIH/NIAAA/1R15AAA019816–01A1, and 2G12 RR003048 RCMI/NCRR/NIH.