During the Antioxidants 2014 World Congress in Paris next June 2014, Dr Namakkal S. Rajasekaran from University of Utah School of Medicine, USA will proposes his work based on Targeting Reductive Stress Strategies.
According Dr Rajasekaran, mutant protein aggregation (PA) cardiomyopathy (MPAC) is characterized by reductive stress (RS) and ventricular dysfunction in humanized mice expressing human mutant CryAB. Sustained activation of nuclear erythroid-2 like factor-2 (Nrf2) causes RS and contributes to proteotoxic cardiac disease. My presentation will discuss (i) whether disrupting Nrf2-antioxidant signaling prevents RS and rescues redox homeostasis in hearts with protein aggregation and (ii) related mechanisms that could delay proteotoxic cardiac disease. We found that Nrf2 deficiency rescues redox homeostasis, which reduces aggregation of mutant proteins and delay the proteotoxic pathological cardiac remodeling.
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