ArticleThe Journal of biological chemistry2013
Loss of cardiolipin leads to perturbation of mitochondrial and cellular iron homeostasis.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- The impact of citicoline on brain mitochondrial dysfunction induced in rats after head irradiation.Scientific reports · 2025Article
- Neddylation inhibition prevents acetaminophen-induced liver damage by enhancing the anabolic cardiolipin pathway.Cell reports. Medicine · 2024Article
- Perturbations in mitochondrial metabolism associated with defective cardiolipin biosynthesis: AnbioRxiv : the preprint server for biology · 2024Article
- Article
- 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
- Conformational changes in the yeast mitochondrial ABC transporter Atm1 during the transport cycle.Science advances · 2021Article
- Cardiolipin, Mitochondria, and Neurological Disease.Trends in endocrinology and metabolism: TEM · 2021Review
- Cardiolipin deficiency in Barth syndrome is not associated with increased superoxide/HFEBS letters · 2021Article
- Studying Lipid-Related Pathophysiology Using the Yeast Model.Frontiers in physiology · 2021Review
- Exploring Yeast as a Study Model of Pantothenate Kinase-Associated Neurodegeneration and for the Identification of Therapeutic Compounds.International journal of molecular sciences · 2020Article
- Metabolic Alterations Caused by Defective Cardiolipin Remodeling in Inherited Cardiomyopathies.Life (Basel, Switzerland) · 2020Review
- Article
- Cardiolipin-deficient cells have decreased levels of the iron-sulfur biogenesis protein frataxin.The Journal of biological chemistry · 2020Article
- Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Article
- Cardiolipin-induced activation of pyruvate dehydrogenase links mitochondrial lipid biosynthesis to TCA cycle function.The Journal of biological chemistry · 2019Article
- Mitochondrial dysfunctions in barth syndrome.IUBMB life · 2019Review
- Cardiolipin-deficient cells depend on anaplerotic pathways to ameliorate defective TCA cycle function.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Article
- Sef1-Regulated Iron Regulon Responds to Mitochondria-Dependent Iron-Sulfur Cluster Biosynthesis inFrontiers in microbiology · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiolipin (CL) is the signature phospholipid of mitochondrial membranes, where it is synthesized locally and plays a critical role in mitochondrial bioenergetic functions. The importance of CL in human health is underscored by the observation that perturbation of CL biosynthesis causes the severe genetic disorder Barth syndrome. To fully understand the cellular response to the loss of CL, we carried out genome-wide expression profiling of the yeast CL mutant crd1Δ. Our results show that the loss of CL in this mutant leads to increased expression of iron uptake genes accompanied by elevated levels of mitochondrial iron and increased sensitivity to iron and hydrogen peroxide. Previous studies have shown that increased mitochondrial iron levels result from perturbations in iron-sulfur (Fe-S) cluster biogenesis. Consistent with an Fe-S defect, deletion of ISU1, one of two ISU genes that encode the mitochondrial Fe-S scaffolding protein essential for the synthesis of Fe-S clusters, led to synthetic growth defects with the crd1Δ mutant. We further show that crd1Δ cells have reduced activities of mitochondrial Fe-S enzymes (aconitase, succinate dehydrogenase, and ubiquinol-cytochrome c oxidoreductase), as well as cytosolic Fe-S enzymes (sulfite reductase and isopropylmalate isomerase). Increased expression of ATM1 or YAP1 did not rescue the Fe-S defects in crd1Δ. These findings show for the first time that CL is required for Fe-S biogenesis to maintain mitochondrial and cellular iron homeostasis.
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