significant downregulation of antioxidant genes (Nqo1, Ho1, Gclm, Cat and Gstα). After RE, the transcript levels of Gclc,. Nqo1, Gsr and Gstα were profoundly ...
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Circulation Abstracts and presentations are embargoed for release at date and time of presentation or time of AHA/ASA news event. Failure to honor embargo policies (http://newsroom.heart.org/newsmedia/embargopolicy) will result in the abstract being withdrawn and barred from presentation. CELLULAR BIOLOGY AND FUNCTION SESSION TITLE: INFLAMMATION IN THE FAILING HEART
Abstract 16369: Nrf2 Deficiency Exacerbates Pathological Cardiac Remodeling in Response to Resistance Exercise GOBINATH SHANMUGAM, Madhusudhanan Narasimhan, Robbie L Conley, Rajesh Kumar Radhakrishnan and Namakkal Soorappan Rajasekaran
Circulation. 2016;134:A16369
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Abstract Introduction: Myocardial remodeling resulting in ventricular hypertrophy and dysfunction are either strongly correlated or causally linked to chronic redox imbalance. Nuclear erythroid2 like factor2 (Nrf2), a master transcriptional regulator plays a major role in cellular redox homeostasis. Here we investigated whether ageassociated decline in Nrf2 is causal to stress induced cardiac remodeling and heart failure. Hypothesis: We hypothesize that genetic ablation or agedependent decline of Nrf2 impairs myocardial redox state and induces pathological ventricular hypertrophy upon resistance exercise (RE). Methods and results: Age and sex matched WT and Nrf2null mice (>22 months; n=6/gp.) were subjected to RE stress for 6 Weeks (25 meter/min, 12% grade) and cardiac functions were assessed by echocardiography and electrocardiogram. Biochemical, cellular and molecular indices related to redox and myocardial structural and functional remodeling were also
analyzed. Results: Pre and post echocardiography analyses in response to RE indicated progressive cardiac hypertrophy in both WT and Nrf2null mice on aging. Interestingly, the degree of cardiac remodeling was significantly higher in Nrf2null when compared to WT mice. Dramatic increase in ejection fraction, cardiac output and R amplitude (V) suggesting that Nrf2 deficiency cause pathological remodeling. Transcriptional signatures of hypertrophy (Anf, Bnf and βMhc) were significantly (p
