ArticleNature metabolism2025
Mitochondrial complex III-derived ROS amplify immunometabolic changes in astrocytes and promote dementia pathology.
Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Experimental workflows for the accurate identification of mitochondrial redox events.Redox biology · 2026Review
- Brain mitochondria as key drivers of cognition and behaviour.Nature reviews. Neuroscience · 2026Review
- Mitochondrial OXPHOS integrates immunometabolic cascade for bone regeneration via coupled ATP production and ROS homeostasis.Redox biology · 2026Article
- Advancing a systems-level understanding of neurodegeneration: the BrightFocus Alzheimer's disease research portfolio.Molecular neurodegeneration · 2026Article
- DRP lyase deficient DNA polymerase beta impairs mitochondrial electron transport chain and compromise mitochondrial DNA integrity.Research square · 2026Article
- The role of mitochondrial Na⁺/Ca²⁺ exchanger in brain cell aging.Journal of bioenergetics and biomembranes · 2026Review
- Postbiotics From Ligilactobacillus salivarius Enhance Mitochondrial Robustness Via TLR2 Signaling in Intestinal Macrophages.Probiotics and antimicrobial proteins · 2026Article
- Nrf2 modulates cytosolic and mitochondrial calcium signal.Redox biology · 2026Article
- Mitochondrial reactive oxygen species regulate HIF-1α stabilization and methylglyoxal accumulation in classically activated mouse macrophages.Immunometabolism (Cobham, Surrey) · 2026Review
- Reprogramming Neuroinflammation: Mitochondrial Targets and Immune Checkpoint Inhibitors in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Astrocytic Redox Homeostasis as a Metabolic Modulator of DNA Damage and Repair in the Ischemic Penumbra.Cells · 2026Review
- Glial fibrillary acidic protein (GFAP) in biofluids: analytical considerations and clinical relevance in neurodegenerative diseases.Journal of neurology · 2026Review
- An engineered ROS-responsive cascade nanoplatform delays Alzheimer's disease progression via Nrf2/GPX4-mediated microglial functional reprogramming.Materials today. Bio · 2026Article
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Pharmacological rescue of mitochondrial dysfunction, neurite degeneration, and premature death of ALS and AD iPSC-derived neurons.bioRxiv : the preprint server for biology · 2026Article
- From Lipids to Mitochondria: Shared Metabolic Alterations in Obesity and Alzheimer's Disease.Cells · 2026Review
- Signaling roles for astrocytic lipid metabolism in brain function.EMBO reports · 2026Review
- Adipose-derived mesenchymal stromal cell-microenvironment interaction network in metabolic syndrome: ADMSC injury response, adaptive regulation, and regenerative potential.Frontiers in cell and developmental biology · 2026Review
- Exercise-induced modulation of astrocyte in Alzheimer's disease: mechanisms and therapeutic implications.Frontiers in physiology · 2026Review
- MECP2 Duplication Uncouples Mitochondrial and Purine Metabolism During neuronal maturation.bioRxiv : the preprint server for biology · 2025Article
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12 authors.
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Abstract
Neurodegenerative disorders alter mitochondrial functions, including the production of reactive oxygen species (ROS). Mitochondrial complex III (CIII) generates ROS implicated in redox signalling, but its triggers, temporal dynamics, targets and disease relevance are not clear. Here, using site-selective suppressors and genetic manipulations together with live mitochondrial ROS imaging and multiomic profiling, we show that CIII is a dominant source of ROS production in astrocytes exposed to neuropathology-related stimuli. Astrocytic CIII ROS production is dependent on nuclear factor-κB and the mitochondrial sodium-calcium exchanger (NCLX) and causes oxidation of select cysteines within immune- and metabolism-associated proteins linked to neurological disease. CIII ROS amplify metabolomic and pathology-associated transcriptional changes in astrocytes, with STAT3 activity as a major mediator, and facilitate neuronal toxicity. Therapeutic suppression of CIII ROS in mice decreases dementia-linked tauopathy and neuroimmune cascades and extends lifespan. Our findings establish CIII ROS as an important immunometabolic signal transducer and tractable therapeutic target in neurodegenerative disease.
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