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Background: Mitochondrial proteins are controlled by glutaredoxin-2 (Grx2)-mediated deglutathionylation reactions. Results: Grx2 deficiency compromises cardiac mitochondrial functions leading to hypertrophy and fibrosis in male mice. This is associated with deregulated glutathionylation reactions and mitochondrial dysfunction. Conclusion: Through deglutathionylation, Grx2 controls mitochondrial oxidative phosphorylation in cardiac muscle. Significance: Deregulated glutathionylation in heart can have pathological consequences.

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