ReviewBiochemical Society transactions2020
Monolysocardiolipin (MLCL) interactions with mitochondrial membrane proteins.
Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Mitochondria as the Hub of Apoptosis: A Comprehensive Insight From Mitochondria to Interactions With Other Organelles.MedComm · 2026Review
- Cross-species evidence for cardiolipin remodeling in neonatal hypoxic-ischemic encephalopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Hydrogen gas with hypothermic machine perfusion induces lipidomic alterations in donation-after-cardiac-death rat livers.Journal of lipid research · 2026Article
- Saturated cardiolipins are potent disruptors of inner mitochondrial membrane structure and function.bioRxiv : the preprint server for biology · 2026Article
- Article
- Adaptive mechanisms in pancreatic islets counteract mitochondrial dysfunction in Barth syndrome.Diabetologia · 2026Article
- Targeting High-Density Aromatic Peptides to Cardiolipin Optimizes the Mitochondrial Membrane Potential and Inhibits Oxidative Stress.FASEB bioAdvances · 2025Article
- Granulopoietic Dysregulation in a Patient-Tailored Mouse Model of Barth Syndrome.Stem cell reviews and reports · 2025Article
- Cardiolipin dynamics promote membrane remodeling by mitochondrial OPA1.Nature communications · 2025Article
- Article
- The role of cardiolipin in mitochondrial dynamics and quality control in neuronal ischemia/reperfusion injury.Cell death & disease · 2025Review
- Barth Syndrome:Genes · 2025Review
- What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025Article
- Annonaceous acetogenins mimic AA005 targets mitochondrial trifunctional enzyme alpha subunit to treat obesity in male mice.Nature communications · 2024Article
- 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
- A Barth Syndrome Patient-DerivedInternational journal of molecular sciences · 2024Article
- Compartmentalized mitochondrial ferroptosis converges with optineurin-mediated mitophagy to impact airway epithelial cell phenotypes and asthma outcomes.Nature communications · 2024Article
- Reduced protein kinase C delta in a high molecular weight complex in mitochondria and elevated creatine uptake into Barth syndrome B lymphoblasts.Journal of translational genetics and genomics · 2024Article
- Anomalous peroxidase activity of cytochrome c is the primary pathogenic target in Barth syndrome.Nature metabolism · 2023Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Monolysocardiolipin (MLCL) is a three-tailed variant of cardiolipin (CL), the signature lipid of mitochondria. MLCL is not normally found in healthy tissue but accumulates in mitochondria of people with Barth syndrome (BTHS), with an overall increase in the MLCL:CL ratio. The reason for MLCL accumulation remains to be fully understood. The effect of MLCL build-up and decreased CL content in causing the characteristics of BTHS are also unclear. In both cases, an understanding of the nature of MLCL interaction with mitochondrial proteins will be key. Recent work has shown that MLCL associates less tightly than CL with proteins in the mitochondrial inner membrane, suggesting that MLCL accumulation is a result of CL degradation, and that the lack of MLCL-protein interactions compromises the stability of the protein-dense mitochondrial inner membrane, leading to a decrease in optimal respiration. There is some data on MLCL-protein interactions for proteins involved in the respiratory chain and in apoptosis, but there remains much to be understood regarding the nature of MLCL-protein interactions. Recent developments in structural, analytical and computational approaches mean that these investigations are now possible. Such an understanding will be key to further insights into how MLCL accumulation impacts mitochondrial membranes. In turn, these insights will help to support the development of therapies for people with BTHS and give a broader understanding of other diseases involving defective CL content.
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