ArticleNature cell biology2013
Cardiolipin externalization to the outer mitochondrial membrane acts as an elimination signal for mitophagy in neuronal cells.
Article in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 653 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
653 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,014 citations in OpenAlex.
- The Intersection of Mitophagy and Autism Spectrum Disorder: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Global trends and perspectives in mitophagy on neurodegenerative diseases: a scientometric analysis over 20 years.Frontiers in medicine · 2025Pooled it
- Targeting mitochondrial quality control in diabetic kidney disease: emerging therapeutic opportunities.Renal failure · 2026Review
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- Mitochondrial Quality Control Links Exercise to Sterile Inflammation in the Cardiovascular System: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- The lipidomic atlas for cellular organelles to reveal the central role of mitochondria in organelle communication.Science China. Life sciences · 2026Article
- Mitophagy in neuronal health and disease: from mechanisms to neurodegeneration.The Journal of clinical investigation · 2026Review
- Mitochondrial CaAntioxidants (Basel, Switzerland) · 2026Article
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026Review
- The Role of Cytochrome P450 Holoenzyme Metabolism in the Origin of Neuropathologies.International journal of molecular sciences · 2026Review
- Circulating Extracellular Mitochondria Perpetuate Endothelial Damage via Cardiolipin-Mediated Mitophagic Overload.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Lipid Metabolism in Central Nervous System Diseases: Pathological Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- ADT-OH promotes mitophagy and suppresses the cytosolic mtDNA-cGAS-STING inflammatory cascade in microglia.Acta pharmacologica Sinica · 2026Article
- Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Disrupted Mitochondrial Quality Control in Atherosclerotic Disease: Mitophagy and Dynamics in Focus.JACC. Basic to translational science · 2026Review
- Cardiolipin as a Signaling Hub: Evolutionary Conservation and Programmable Platforms Coupling Mitochondrial Stress to Cell Fate.International journal of molecular sciences · 2026Review
- Membrane Models and the Pursuit of Coherence.Biochemistry · 2026Review
- Rethinking photosensitization in therapy and sun protection.Chemical science · 2026Review
593 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
26 authors at 1 institution in 1 country.
Funding
Abstract
Recognition of injured mitochondria for degradation by macroautophagy is essential for cellular health, but the mechanisms remain poorly understood. Cardiolipin is an inner mitochondrial membrane phospholipid. We found that rotenone, staurosporine, 6-hydroxydopamine and other pro-mitophagy stimuli caused externalization of cardiolipin to the mitochondrial surface in primary cortical neurons and SH-SY5Y cells. RNAi knockdown of cardiolipin synthase or of phospholipid scramblase-3, which transports cardiolipin to the outer mitochondrial membrane, decreased the delivery of mitochondria to autophagosomes. Furthermore, we found that the autophagy protein microtubule-associated-protein-1 light chain 3 (LC3), which mediates both autophagosome formation and cargo recognition, contains cardiolipin-binding sites important for the engulfment of mitochondria by the autophagic system. Mutation of LC3 residues predicted as cardiolipin-interaction sites by computational modelling inhibited its participation in mitophagy. These data indicate that redistribution of cardiolipin serves as an 'eat-me' signal for the elimination of damaged mitochondria from neuronal cells.
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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.