Targeted overexpression of catalase to mitochondria does not prevent cardioskeletal myopathy in Barth syndrome

Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans

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Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and heart-on-chip technologies

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A novel X-linked gene, G4.5. is responsible for Barth syndrome

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Mendelian Disorder, Genetic Disorder, Genetics +6

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Overexpression of Catalase Targeted to Mitochondria Attenuates Murine Cardiac Aging

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