ArticleOxidative medicine and cellular longevity2014
Mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes.
Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Adaptive mechanisms in pancreatic islets counteract mitochondrial dysfunction in Barth syndrome.Diabetologia · 2026Article
- What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025Article
- Cyclohexylalanine-Containing α-Helical Amphipathic Peptide Targets Cardiolipin, Rescuing Mitochondrial Dysfunction in Kidney Injury.Journal of medicinal chemistry · 2024Article
- Mitochondrial Dysfunction, Oxidative Stress, and Therapeutic Strategies in Diabetes, Obesity, and Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Resveratrol-Mediated Reversal of Doxorubicin-Induced Osteoclast Differentiation.International journal of molecular sciences · 2022Article
- Regular Supplementation with Antioxidants Rescues Doxorubicin-Induced Bone Deformities and Mineralization Delay in Zebrafish.Nutrients · 2022Article
- NAD supplementation improves mitochondrial performance of cardiolipin mutants.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022Article
- Reversal of Doxorubicin-Induced Bone Loss and Mineralization by Supplementation of Resveratrol and MitoTEMPO in the Early Development ofNutrients · 2022Article
- Barth syndrome cardiomyopathy: targeting the mitochondria with elamipretide.Heart failure reviews · 2021Review
- Barth syndrome: cardiolipin, cellular pathophysiology, management, and novel therapeutic targets.Molecular and cellular biochemistry · 2021Review
- Cardiolipin deficiency in Barth syndrome is not associated with increased superoxide/HFEBS letters · 2021Article
- Mitochondrial Quality Control in the Maintenance of Cardiovascular Homeostasis: The Roles and Interregulation of UPS, Mitochondrial Dynamics and Mitophagy.Oxidative medicine and cellular longevity · 2021Review
- Mitophagy in Diabetic Cardiomyopathy: Roles and Mechanisms.Frontiers in cell and developmental biology · 2021Review
- Metabolic Alterations Caused by Defective Cardiolipin Remodeling in Inherited Cardiomyopathies.Life (Basel, Switzerland) · 2020Review
- Mitochondrial CaActa pharmacologica Sinica · 2020Review
- Tafazzin deficiency impairs CoA-dependent oxidative metabolism in cardiac mitochondria.The Journal of biological chemistry · 2020Article
- Review
- Barth Syndrome: Exploring Cardiac Metabolism with Induced Pluripotent Stem Cell-Derived Cardiomyocytes.Metabolites · 2019Article
- Imbalanced mitochondrial function provokes heterotaxy via aberrant ciliogenesis.The Journal of clinical investigation · 2019Article
- Genetic ablation of TAZ induces HepG2 liver cancer cell apoptosis through activating the CaMKII/MIEF1 signaling pathway.OncoTargets and therapy · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tafazzin, a mitochondrial acyltransferase, plays an important role in cardiolipin side chain remodeling. Previous studies have shown that dysfunction of tafazzin reduces cardiolipin content, impairs mitochondrial function, and causes dilated cardiomyopathy in Barth syndrome. Reactive oxygen species (ROS) have been implicated in the development of cardiomyopathy and are also the obligated byproducts of mitochondria. We hypothesized that tafazzin knockdown increases ROS production from mitochondria, and a mitochondria-targeted antioxidant prevents tafazzin knockdown induced mitochondrial and cardiac dysfunction. We employed cardiac myocytes transduced with an adenovirus containing tafazzin shRNA as a model to investigate the effects of the mitochondrial antioxidant, mito-Tempo. Knocking down tafazzin decreased steady state levels of cardiolipin and increased mitochondrial ROS. Treatment of cardiac myocytes with mito-Tempo normalized tafazzin knockdown enhanced mitochondrial ROS production and cellular ATP decline. Mito-Tempo also significantly abrogated tafazzin knockdown induced cardiac hypertrophy, contractile dysfunction, and cell death. We conclude that mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes and suggest mito-Tempo as a potential therapeutic for Barth syndrome and other dilated cardiomyopathies resulting from mitochondrial oxidative stress.
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