ArticleScientific reports2024
SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Revisiting Inherited Metabolic Diseases (IMDs) Through the Lens of Selective Autophagy.Journal of inherited metabolic disease · 2026Review
- Mitochondrial Quality Control in Inherited Mitochondrial Cardiomyopathy: Convergent Pathobiology and a Testable Therapeutic Framework.International journal of molecular sciences · 2026Review
- Mitochondrial Toxicology of Heavy Metals and Pesticides: Transport Systems, Mitochondrial Dysfunction and Permeability Transition.International journal of molecular sciences · 2026Review
- LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia.Redox biology · 2026Review
- Disturbed mitochondrial maturation in cardiolipin remodeling-deficient cardiomyocytes.iScience · 2026Article
- Review
- Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Adaptive mechanisms in pancreatic islets counteract mitochondrial dysfunction in Barth syndrome.Diabetologia · 2026Article
- Defective vascular smooth muscle cell tafazzin impairs mitochondrial function and promotes atherosclerosis in preclinical models.Nature communications · 2025Article
- Mechano-energetic uncoupling in heart failure.Nature reviews. Cardiology · 2025Review
- Targeting High-Density Aromatic Peptides to Cardiolipin Optimizes the Mitochondrial Membrane Potential and Inhibits Oxidative Stress.FASEB bioAdvances · 2025Article
- Contemporary insights into elamipretide's mitochondrial mechanism of action and therapeutic effects.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Article
- Elamipretide: A Review of Its Structure, Mechanism of Action, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Mitochondrial dysfunction as a therapeutic nexus in HFpEF: therapeutic target and pharmacological advances.Frontiers in pharmacology · 2025Review
- What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025Article
- The mitochondrial-targeted peptide therapeutic elamipretide improves cardiac and skeletal muscle function during aging without detectable changes in tissue epigenetic or transcriptomic age.bioRxiv : the preprint server for biology · 2024Article
- Lhx6 deficiency causes human embryonic palatal mesenchymal cell mitophagy dysfunction in cleft palate.Molecular medicine (Cambridge, Mass.) · 2024Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Barth syndrome (BTHS) is a lethal rare genetic disorder, which results in cardiac dysfunction, severe skeletal muscle weakness, immune issues and growth delay. Mutations in the TAFAZZIN gene, which is responsible for the remodeling of the phospholipid cardiolipin (CL), lead to abnormalities in mitochondrial membrane, including alteration of mature CL acyl composition and the presence of monolysocardiolipin (MLCL). The dramatic increase in the MLCL/CL ratio is the hallmark of patients with BTHS, which is associated with mitochondrial bioenergetics dysfunction and altered membrane ultrastructure. There are currently no specific therapies for BTHS. Here, we showed that cardiac mitochondria isolated from TAFAZZIN knockdown (Taz
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