ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2021
Effects of O-GlcNAcylation on functional mitochondrial transfer from astrocytes.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Astrocyte Senescence Disrupts the Extracellular Mitochondrial Compartment and Compromises Bioenergetic Support to Human Neurons.Antioxidants (Basel, Switzerland) · 2026Article
- Intriguing role of the Golgi apparatus in astrocyte function: Implications for disorders.Neural regeneration research · 2026Article
- Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.Translational stroke research · 2026Review
- Astrocytic mitochondrial transfer: a new horizon for metabolic rescue and precision therapy in ischemic stroke.Journal of translational medicine · 2026Review
- The role of mitochondrial transfer in lung disease.Respiratory research · 2025Review
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Effects of mitochondrial O-GlcNAcylation in pericytes after mechanical injury.Brain research · 2025Article
- Aerobic exercise improves astrocyte mitochondrial quality and transfer to neurons in a mouse model of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- Pharmacologically increasing O-GlcNAcylation increases complexity of astrocytes in the dentate gyrus of TgF344-AD rats.Frontiers in aging neuroscience · 2025Article
- O-linked β-N-acetylglucosamine modification in diabetic foot ulcer pathogenesis.Burns & trauma · 2025Review
- Regulation of blood-brain barrier integrity byScience advances · 2024Article
- The Role of Astrocytic Mitochondria in the Pathogenesis of Brain Ischemia.Molecular neurobiology · 2024Review
- O-GlcNAcylation: a pro-survival response to acute stress in the cardiovascular and central nervous systems.European journal of medical research · 2024Review
- O-GlcNAcylation is essential for therapeutic mitochondrial transplantation.Communications medicine · 2023Article
- The Involvement of Neuroinflammation in the Onset and Progression of Parkinson's Disease.International journal of molecular sciences · 2023Review
- Leveraging single-cell RNA sequencing to unravel the impact of aging on stroke recovery mechanisms in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Astrocytic mitochondrial frataxin-A promising target for ischemic brain injury.CNS neuroscience & therapeutics · 2023Review
- Exploring the therapeutic potential of the mitochondrial transfer-associated enzymatic machinery in brain degeneration.Frontiers in physiology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria may be transferred from cell to cell in the central nervous system and this process may help defend neurons against injury and disease. But how mitochondria maintain their functionality during the process of release into extracellular space remains unknown. Here, we report that mitochondrial protein O-GlcNAcylation is a critical process to support extracellular mitochondrial functionality. Activation of CD38-cADPR signaling in astrocytes robustly induced protein O-GlcNAcylation in mitochondria, while oxygen-glucose deprivation and reoxygenation showed transient and mild protein modification. Blocking the endoplasmic reticulum - Golgi trafficking with Brefeldin A or slc35B4 siRNA reduced O-GlcNAcylation, and resulted in the secretion of mitochondria with decreased membrane potential and mtDNA. Finally, loss-of-function studies verified that O-GlcNAc-modified mitochondria demonstrated higher levels of neuroprotection after astrocyte-to-neuron mitochondrial transfer. Collectively, these findings suggest that post-translational modification by O-GlcNAc may be required for supporting the functionality and neuroprotective properties of mitochondria released from astrocytes.
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What OpenQuestion holds
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.