ArticleDevelopmental cell2024
Slc25a3-dependent copper transport controls flickering-induced Opa1 processing for mitochondrial safeguard.
Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Mitochondrial Dynamics and SLC25 Transporters in Neurodegeneration: From Mechanisms to Therapeutic Opportunities.Biomolecules · 2026Review
- Copper transport to mitochondria by SLC25A3 contributes to skeletal myoblast differentiation and is required for survival of differentiated myotubes.bioRxiv : the preprint server for biology · 2026Article
- Article
- Mitochondrial Fission and Fusion Disorders and Autophagy Abnormalities in Parkinson's Disease.Neurochemical research · 2026Review
- Tackling cuproptosis: from metabolic rewiring to therapeutic exploitation in cancer.Cellular & molecular immunology · 2026Review
- Dietary chromium picolinate-promoted oxidative phosphorylation may be a potential mean to improve hypoxia tolerance of juvenile grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Context-dependent inhibitory roles of RhoA in 3D invasive cell migration within the extracellular matrix.Cell reports · 2025Article
- Blockade of mitochondrial components release by exosome pathway promotes the pathogenesis of Fuchs endothelial corneal dystrophy.Cell death discovery · 2025Article
- Novel Evolutionarily Conserved Oncogene COA4 is Driven by KRAS Mutant and Promotes Cancer Metastasis Through Dual Mitochondrial Metabolism-Dependent and -Independent Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting mitochondrial structure and dynamics for therapeutic intervention in cancer.PLoS biology · 2025Article
- Copper Chelation Induces Morphology Change in Mitochondria of Triple-Negative Breast Cancer.JACS Au · 2025Article
- HThe Journal of biological chemistry · 2025Article
- Copper doped bioactive glass promotes matrix vesicles-mediated biomineralization via osteoblast mitophagy and mitochondrial dynamics during bone regeneration.Bioactive materials · 2025Article
- Chinese sacbrood virus mediates m6A modification to target and suppress the expression of hemolymph maintenance gene AF9, exacerbating bee infections.Journal of virology · 2025Article
- Macrophage-derived mitochondria-rich extracellular vesicles aggravate bone loss in periodontitis by disrupting the mitochondrial dynamics of BMSCs.Journal of nanobiotechnology · 2025Article
- Article
- Copper metabolism in hepatocellular carcinoma: from molecular mechanisms to therapeutic opportunities.Frontiers in molecular biosciences · 2025Review
- Mammalian copper homeostasis: physiological roles and molecular mechanisms.Physiological reviews · 2025Review
- Aconiti Lateralis Radix Praeparata ameliorates heart failure via PI3K/AKT/Bnip3 pathway.Frontiers in pharmacology · 2025Article
- GRHL2-HER3 and E-cadherin mediate EGFR-bypass drug resistance in lung cancer cells.Frontiers in cell and developmental biology · 2024Article
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Authors and funding
5 authors.
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Abstract
Following the Goldilocks principle, mitochondria size must be "just right." Mitochondria balance division and fusion to avoid becoming too big or too small. Defects in this balance produce dysfunctional mitochondria in human diseases. Mitochondrial safeguard (MitoSafe) is a defense mechanism that protects mitochondria against extreme enlarging by suppressing fusion in mammalian cells. In MitoSafe, hyperfused mitochondria elicit flickering-short pulses of mitochondrial depolarization. Flickering activates an inner membrane protease, Oma1, which in turn proteolytically inactivates a mitochondrial fusion protein, Opa1. The mechanisms underlying flickering are unknown. Using a live-imaging screen, we identified Slc25a3 (a mitochondrial carrier transporting phosphate and copper) as necessary for flickering and Opa1 cleavage. Remarkably, copper, but not phosphate, is critical for flickering. Furthermore, we found that two copper-containing mitochondrial enzymes, superoxide dismutase 1 and cytochrome c oxidase, regulate flickering. Our data identify an unforeseen mechanism linking copper, redox homeostasis, and membrane flickering in mitochondrial defense against deleterious fusion.
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