ArticleNature metabolism2023
Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions.
Article in Nature metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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Who cites it
29 citing papers in PubMed, 66 citations in OpenAlex.
- A Micropeptide Component of the OGDH Complex Modulates ATP Production in the TCA Cycle.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Immunometabolic reprogramming in multiple sclerosis: from pathogenic amplifier to therapeutic target in neuroinflammation and remyelination.Inflammopharmacology · 2026Review
- Multi-Targeted Neuroprotection byInternational journal of molecular sciences · 2026Article
- Integrated proteogenomic profiling reveals coordinated differential expression signatures during neuroinflammation.Acta neuropathologica communications · 2026Article
- Exercise mimetics: molecular mechanisms, biological and therapeutic effects.Molecular biomedicine · 2026Review
- Spinal cord imaging in preclinical research.Neural regeneration research · 2026Article
- Mechanisms by Which Exercise Delays Brain Aging Through Regulation of the Mitochondrial Quality Control System.Biology · 2026Review
- Integrated Transcriptomic and Metabolomic Analysis Deciphers the Molecular and Metabolic Mechanisms Underlying Growth Rate Divergence in Dezhou Donkeys.Animals : an open access journal from MDPI · 2026Article
- Malic enzyme 2 suppresses PINK1-Parkin-mediated mitophagy by stabilizing ATAD3A via competitive interaction with TRIM25.Cell death & disease · 2026Article
- Adipose tissue-derived stromal cells enhance glycolytic metabolism in injured nerve cells via the FOXK1-HK2 axis for spinal cord injury repair.Journal of translational medicine · 2026Article
- Bioengineered ROS-tolerant probiotic reshapes gut microbiota-host axis to ameliorate type 2 diabetes in male mice.Nature communications · 2026Article
- Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Metabolic reprogramming in sepsis-associated encephalopathy: emerging mechanisms, candidate biomarkers, and future therapeutic directions.Frontiers in medicine · 2026Review
- Alpha Ketoglutaric Acid attenuates LPS Induced Inflammatory Response by Inhibiting the PKCε/MAPK/P65 Signaling Pathway and Inhibit Oxidative Stress in Kupffer Cells.Inflammation · 2025Article
- Comprehensive and In-Depth Molecular and Pathway Studies of the Hippocampus in Alzheimer's Disease.Cellular and molecular neurobiology · 2025Article
- Dysregulation of cellular metabolism within the gut-brain axis is associated with behavioural changes in chronic intestinal inflammation.Journal of neuroinflammation · 2025Article
- Enhancement of spinal cord injury repair in rats using photo-crosslinked GelMA hydrogel combined with mitochondrial transplantation.Bioengineering & translational medicine · 2025Article
- AAV-based delivery of RNAi targeting ataxin-2 improves survival and pathology in TDP-43 mice.Nature communications · 2025Article
- Genetically encoded biosensors of metabolic function for the study of neurodegeneration, a review and perspective.Neurophotonics · 2025Review
- Advances in research on mitochondrial dysfunction in neurodegenerative diseases.Journal of neurology · 2025Review
Corrections and comments
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Authors and funding
24 authors at 11 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation in the central nervous system can impair the function of neuronal mitochondria and contributes to axon degeneration in the common neuroinflammatory disease multiple sclerosis (MS). Here we combine cell-type-specific mitochondrial proteomics with in vivo biosensor imaging to dissect how inflammation alters the molecular composition and functional capacity of neuronal mitochondria. We show that neuroinflammatory lesions in the mouse spinal cord cause widespread and persisting axonal ATP deficiency, which precedes mitochondrial oxidation and calcium overload. This axonal energy deficiency is associated with impaired electron transport chain function, but also an upstream imbalance of tricarboxylic acid (TCA) cycle enzymes, with several, including key rate-limiting, enzymes being depleted in neuronal mitochondria in experimental models and in MS lesions. Notably, viral overexpression of individual TCA enzymes can ameliorate the axonal energy deficits in neuroinflammatory lesions, suggesting that TCA cycle dysfunction in MS may be amendable to therapy.
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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.