ReviewJournal of molecular biology2020
The Function of Tafazzin, a Mitochondrial Phospholipid-Lysophospholipid Acyltransferase.
Review in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- Running rich: how excess fatty acid oxidation drains the cardiac engine.The Journal of clinical investigation · 2026Article
- Cristae: bridging bioenergetic hubs and compartmental barriers in mitochondrial homeostasis.Cell death & disease · 2026Review
- Src-mediated PHB2 phosphorylation disrupts mitochondrial cristae through cardiolipin dissociation in hepatocellular carcinoma.Redox biology · 2026Article
- Article
- Article
- Barth Syndrome:Genes · 2025Review
- De-succinylation-induced accumulation of TRMT10C in the nucleus plays a detrimental role in coronary microembolization via its m1A modification function.International journal of biological sciences · 2025Article
- Setting the curve: the biophysical properties of lipids in mitochondrial form and function.Journal of lipid research · 2024Review
- Functional diversity among cardiolipin binding sites on the mitochondrial ADP/ATP carrier.The EMBO journal · 2024Article
- SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome.Scientific reports · 2024Article
- Intersection of Immunology and Metabolism in Myocardial Disease.Circulation research · 2024Review
- Review
- Tafazzin mediates tamoxifen resistance by regulating cellular phospholipid composition in ER-positive breast cancer.Cancer gene therapy · 2024Article
- SIRT3 regulates cardiolipin biosynthesis in pressure overload-induced cardiac remodeling by PPARγ-mediated mechanism.PloS one · 2024Article
- Article
- Spatial Lipidomics Reveals Lipid Changes in the Cotyledon and Plumule of Mung Bean Seeds during Germination.Journal of agricultural and food chemistry · 2023Article
- The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- Extracellular vesicles, the emerging mirrors of brain physiopathology.International journal of biological sciences · 2023Review
- Case report: Variability in clinical features as a potential pitfall for the diagnosis of Barth syndrome.Frontiers in pediatrics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tafazzin is a mitochondrial enzyme that exchanges fatty acids between phospholipids by phospholipid-lysophospholipid transacylation. The reaction alters the molecular species composition and, as a result, the physical properties of lipids. In vivo, the most important substrate of tafazzin is the mitochondria-specific lipid cardiolipin. Tafazzin mutations cause the human disease Barth syndrome, which presents with cardiomyopathy, skeletal muscle weakness, fatigue, and other symptoms, probably all related to mitochondrial dysfunction. The reason why mitochondria require tafazzin is still not known, but recent evidence suggests that tafazzin may lower the energy cost associated with protein crowding in the inner mitochondrial membrane.
Indexed as
Identifiers
What OpenQuestion holds
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.