ArticleJournal of molecular and cellular cardiology2018
Targeted overexpression of catalase to mitochondria does not prevent cardioskeletal myopathy in Barth syndrome.
Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Article
- Deficient Cardiolipin Remodelling Alters Muscle Fibre Composition and Neuromuscular Connectivity in Barth Syndrome.Journal of cachexia, sarcopenia and muscle · 2026Article
- Deficient Cardiolipin Remodeling Alters Muscle Fiber Composition and Neuromuscular Connectivity in Barth Syndrome.bioRxiv : the preprint server for biology · 2025Article
- Acute mitochondrial reactive oxygen species emissions drive mitochondrial dysfunction after traumatic muscle injury in male mice.American journal of physiology. Cell physiology · 2025Article
- Allogenic mitochondria transfer improves cardiac function in iPS-cell-differentiated cardiomyocytes of a patient with Barth syndrome.Experimental & molecular medicine · 2025Article
- What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025Article
- Pharmacological increases in circulating ketones fail to alleviate the hypertrophic cardiomyopathy present in the Tafazzin knockdown mouse model of Barth syndrome.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2025Article
- Mitochondrial membrane lipids in the regulation of bioenergetic flux.Cell metabolism · 2024Review
- Inhibition of the skeletal muscle Lands cycle ameliorates weakness induced by physical inactivity.Journal of cachexia, sarcopenia and muscle · 2024Article
- Lipid peroxidation does not mediate muscle atrophy induced by PSD deficiency.bioRxiv : the preprint server for biology · 2023Article
- Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome.Basic research in cardiology · 2023Article
- SMYD1a protects the heart from ischemic injury by regulating OPA1-mediated cristae remodeling and supercomplex formation.Basic research in cardiology · 2023Article
- Weight loss increases skeletal muscle mitochondrial energy efficiency in obese mice.Life metabolism · 2023Article
- Phenotypic Characterization of MaleBiomedicines · 2023Article
- Chicken or Egg? Mitochondrial Phospholipids and Oxidative Stress in Disuse-Induced Skeletal Muscle Atrophy.Antioxidants & redox signaling · 2023Review
- Cardiac Involvement in Mitochondrial Disorders.Current heart failure reports · 2023Review
- EFHD1 ablation inhibits cardiac mitoflash activation and protects cardiomyocytes from ischemia.Journal of molecular and cellular cardiology · 2022Article
- Barth Syndrome Cardiomyopathy: An Update.Genes · 2022Review
- Article
- Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022Review
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Authors and funding
9 authors.
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Abstract
Barth Syndrome (BTHS) is an X-linked recessive disorder characterized by cardiomyopathy and muscle weakness. The underlying cause of BTHS is a mutation in the tafazzin (TAZ) gene, a key enzyme of cardiolipin biosynthesis. The lack of CL arising from loss of TAZ function results in destabilization of the electron transport system, promoting oxidative stress that is thought to contribute to development of cardioskeletal myopathy. Indeed, in vitro studies demonstrate that mitochondria-targeted antioxidants improve contractile capacity in TAZ-deficient cardiomyocytes. The purpose of the present study was to determine if resolving mitochondrial oxidative stress would be sufficient to prevent cardiomyopathy and skeletal myopathy in vivo using a mouse model of BTHS. To this end we crossed mice that overexpress catalase in the mitochondria (MCAT mice) with TAZ-deficient mice (TAZKD) to produce TAZKD mice that selectively overexpress catalase in the mitochondria (TAZKD+MCAT mice). TAZKD+MCAT mice exhibited decreased mitochondrial H
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