ReviewJournal of inherited metabolic disease2022
Cardiolipin function in the yeast S. cerevisiae and the lessons learned for 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 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Combinatorial engineering approaches for improved lipid production in Saccharomyces cerevisiae.FEMS yeast research · 2026Article
- Mitochondrial dysfunction and lipid dysregulation in yeast lacking phosphatidylserine.Molecular biology of the cell · 2025Article
- Barth Syndrome:Genes · 2025Review
- Cardiolipin remodeling maintains the inner mitochondrial membrane in cells with saturated lipidomes.Journal of lipid research · 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
- Unraveling the mechanisms of cardiolipin function: The role of oxidative polymerization of unsaturated acyl chains.Redox biology · 2023Article
- PKA regulatory subunit Bcy1 couples growth, lipid metabolism, and fermentation during anaerobic xylose growth in Saccharomyces cerevisiae.PLoS genetics · 2023Article
- The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- Insights into complex I assembly: Function of NDUFAF1 and a link with cardiolipin remodeling.Science advances · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiolipin (CL) is the signature phospholipid (PL) of mitochondria and plays a pivotal role in mitochondrial and cellular function. Disruption of the CL remodeling gene tafazzin (TAZ) causes the severe genetic disorder Barth syndrome (BTHS). Our current understanding of the function of CL and the mechanism underlying the disease has greatly benefited from studies utilizing the powerful yeast model Saccharomyces cerevisiae. In this review, we discuss important findings on the function of CL and its remodeling from yeast studies and the implications of these findings for BTHS, highlighting the potential physiological modifiers that may contribute to the disparities in clinical presentation among BTHS patients.
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Registered trials
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