ArticleBiochimica et biophysica acta. Molecular and cell biology of lipids2018
Loss of tafazzin results in decreased myoblast differentiation in C2C12 cells: A myoblast model of Barth syndrome and cardiolipin deficiency.
Article in Biochimica et biophysica acta. Molecular and cell biology of lipids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 41 citations in OpenAlex.
- Omega-3 fatty acid supplementation improves skeletal muscle mitochondrial function in a model of Barth syndrome.JCI insight · 2026Article
- Loss of TAFAZZIN leads to perturbation of amino acid metabolism and reduction of collagen synthesis.bioRxiv : the preprint server for biology · 2026Article
- Saturated cardiolipins are potent disruptors of inner mitochondrial membrane structure and function.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025Article
- Upregulation of the AMPK-FOXO1-PDK4 pathway is a primary mechanism of pyruvate dehydrogenase activity reduction in tafazzin-deficient cells.Scientific reports · 2024Article
- HOIL-1L deficiency induces cell cycle alteration which causes immaturity of skeletal muscle and cardiomyocytes.Scientific reports · 2024Article
- Phosphorylation of cell cycle and apoptosis regulatory protein-1 by stress activated protein kinase P38γ is a novel mechanism of apoptosis signaling by genotoxic chemotherapy.Frontiers in oncology · 2024Article
- Anomalous peroxidase activity of cytochrome c is the primary pathogenic target in Barth syndrome.Nature metabolism · 2023Article
- Mitochondrial phospholipid metabolism in health and disease.Journal of cell science · 2023Article
- The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- Chicken or Egg? Mitochondrial Phospholipids and Oxidative Stress in Disuse-Induced Skeletal Muscle Atrophy.Antioxidants & redox signaling · 2023Review
- Mechanical characterization of isolated mitochondria under conditions of oxidative stress.Biomicrofluidics · 2022Article
- Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management.Cells · 2022Review
- Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- NAD supplementation improves mitochondrial performance of cardiolipin mutants.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022Article
- Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022Review
- Cardiolipin function in the yeast S. cerevisiae and the lessons learned for Barth syndrome.Journal of inherited metabolic disease · 2022Review
- Current Knowledge on the Role of Cardiolipin Remodeling in the Context of Lipid Oxidation and Barth Syndrome.Frontiers in molecular biosciences · 2022Article
- Cardiolipin deficiency in Barth syndrome is not associated with increased superoxide/HFEBS letters · 2021Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Barth syndrome (BTHS) is an X-linked genetic disorder resulting from mutations in the tafazzin gene (TAZ), which encodes the transacylase that remodels the mitochondrial phospholipid cardiolipin (CL). While most BTHS patients exhibit pronounced skeletal myopathy, the mechanisms linking defective CL remodeling and skeletal myopathy have not been determined. In this study, we constructed a CRISPR-generated stable tafazzin knockout (TAZ-KO) C2C12 myoblast cell line. TAZ-KO cells exhibit mitochondrial deficits consistent with other models of BTHS, including accumulation of monolyso-CL (MLCL), decreased mitochondrial respiration, and increased mitochondrial ROS production. Additionally, tafazzin deficiency was associated with impairment of myocyte differentiation. Future studies should determine whether alterations in myogenic determination contribute to the skeletal myopathy observed in BTHS patients. The BTHS myoblast model will enable studies to elucidate mechanisms by which defective CL remodeling interferes with normal myocyte differentiation and skeletal muscle ontogenesis.
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