Acute Treatment With Antioxidant N-Propionylglycine Attenuates Mitochondrial Cysteine Redox Post-Translational Modifications and Restores Endogenous Antioxidants in the Diabetic Heart, Identified Using Quantitative Mass Spectrometry
Excessive production of reactive oxygen species (ROS) is a powerful shared mechanism in the pathogenesis of cardiovascular disease (CVD) and type 2 Diabetes (T2D). Reactive oxygen species overproduction reduces cellular antioxidant capacity and increases contractile dysfunction through protein oxidation. Clinically, the cumulative effect is increased mortality risk following a single, acute cardiac event in T2D cohorts [1]. Cysteine-containing proteins are at risk of oxidation, with protection afforded by protecting these sites with antioxidant therapies [2].
Source: Heart, Lung and Circulation - Category: Cardiology Authors: M. Talbot, A. Rookyard, D. Li, S. Cordwell, M. White Source Type: research
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