ReviewJournal of inherited metabolic disease2022
Experimental models of Barth syndrome.
Review in Journal of inherited metabolic disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- Disturbed mitochondrial maturation in cardiolipin remodeling-deficient cardiomyocytes.iScience · 2026Article
- Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Metabolic cardiomyopathies: untangling clinical heterogeneity with human stem-cell derived models.EMBO molecular medicine · 2025Review
- Article
- Tafazzin-deficient zebrafish display mitochondrial dysfunction, neutropenia, and metabolic defects without myopathy.Scientific reports · 2025Article
- A murine model of Barth syndrome recapitulates human cardiac and skeletal muscle phenotypes.Disease models & mechanisms · 2025Article
- Setting the curve: the biophysical properties of lipids in mitochondrial form and function.Journal of lipid research · 2024Review
- Cardiolipin remodeling maintains the inner mitochondrial membrane in cells with saturated lipidomes.Journal of lipid research · 2024Article
- Estimation of crossbridge-state during cardiomyocyte beating using second harmonic generation.Life science alliance · 2023Article
- A novel panel of Drosophila TAFAZZIN mutants in distinct genetic backgrounds as a resource for therapeutic testing.PloS one · 2023Article
- Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice.Scientific reports · 2022Article
- Barth Syndrome Cardiomyopathy: An Update.Genes · 2022Review
- Re-Expression of Tafazzin Isoforms in TAZ-Deficient C6 Glioma Cells Restores Cardiolipin Composition but Not Proliferation Rate and Alterations in Gene Expression.Frontiers in genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Mutation of the gene Tafazzin (TAZ) causes Barth syndrome, an X-linked disorder characterized by cardiomyopathy, skeletal muscle weakness, and neutropenia. TAZ is an acyltransferase that catalyzes the remodeling of cardiolipin, the signature phospholipid of the inner mitochondrial membrane. Here, we review the major model systems that have been established to study the role of cardiolipin remodeling in mitochondrial function and the pathogenesis of Barth syndrome. We summarize key features of each model and provide examples of how each has contributed to advance our understanding of TAZ function and Barth syndrome pathophysiology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.