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From the Center for Cardiovascular Research (H.Y., B.C.B.), University of Rochester, NY, and Department of Molecular Cardiology (J.H.), University of Frankfurt, Germany.
Correspondence to Bradford C. Berk, MD, PhD, Center for Cardiovascular Research, Box 679, 601 Elmwood Ave, University of Rochester, Rochester, NY 14642. E-mail bradford_berk{at}urmc.rochester.edu
Abstract
The thioredoxin (TRX) system (TRX, TRX reductase, and NADPH) is a ubiquitous thiol oxidoreductase system that regulates cellular reduction/oxidation (redox) status. The oxidation mechanism for disease pathogenesis states that an imbalance in cell redox state alters function of multiple cell pathways. In this study, we review the essential role for TRX to limit oxidative stress directly via antioxidant effects and indirectly by protein-protein interaction with key signaling molecules, such as apoptosis signal-regulating kinase 1. We propose that TRX and its endogenous regulators are important future targets to develop clinical therapies for cardiovascular disorders associated with oxidative stress.
Key Words: antioxidants cardiovascular diseases endothelium smooth muscle signal transduction
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