Purpose of review: Recent studies indicate that an imbalance in cell redox state alters multiple cell pathways that may contribute to the pathogenesis of cardiovascular disorders including hypertension and renal failure.
Recent findings: The thioredoxin system (thioredoxin, thioredoxin reductase, and NADPH) is a ubiquitous thiol oxidoreductase system that regulates cellular reduction/oxidation (redox) status. Thioredoxin plays an essential role in cell function by limiting oxidative stress directly via antioxidant effects and indirectly by protein-protein interactions with key signaling molecules such as thioredoxin-interacting protein (TXNIP). Examples include the findings that hyperglycemia and diabetes induce TXNIP and decrease thioredoxin activity, while steady blood flow decreases TXNIP and increases thioredoxin activity.
Summary: Based on these findings we propose that thioredoxin and its endogenous regulators represent important future targets to develop clinical therapies for diseases associated with oxidative stress.