ArticleBiomedicines2024
Oxygen Glucose Deprivation-Induced Lactylation of H3K9 Contributes to M1 Polarization and Inflammation of Microglia Through TNF Pathway.
Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- H4K12 Lactylation Impairs Dopaminergic Neuron Energy Metabolism via the HIF-1α/NDUFS1 Pathway in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Novel Approach to Neuropathic Pain Treatment: Lactylation Targeting Microglia.Molecular neurobiology · 2026Review
- Lactylation of PTBP1 drives a pro-apoptotic positive feedback loop in microglia following oxygen-glucose deprivation/reoxygenation-induced injury.Cell death & disease · 2026Article
- The Lactate Nexus: A Molecular Bridge Linking Physical Activity, Sleep, and Cognitive Enhancement.Biomedicines · 2026Review
- Esketamine Attenuates Postoperative Neurocognitive Disorder in Aged Mice: Associations with Bioenergetic Remodeling in Hippocampal CD11b-Enriched Cell Fractions and Glycolysis-Related Signaling.Drug design, development and therapy · 2026Article
- Lactylation at the crossroads of metabolism and epigenetics in neuroinflammation.Frontiers in immunology · 2026Review
- From metabolic substrate to epigenetic regulation: roles and mechanisms of lactylation in brain health and disease.Frontiers in molecular neuroscience · 2026Review
- Metabolite-neuro-immune relay in chronic pain: spatial-temporal lactate, succinate and itaconate signalling as drivers of glial reprogramming and neuronal sensitisation.Frontiers in pharmacology · 2026Review
- Unraveling the role of lactylation in cell death and correlative diseases: a comprehensive review.Frontiers in cell and developmental biology · 2026Review
- Regulatory Landscapes of Protein Acylations in Neuroinflammation: From Molecular Mechanisms to Therapeutic Targets.Neurochemical research · 2025Review
- Beyond Fuel: Exercise-Induced Lactate as a Metabolic-Epigenetic Regulator in Central Nervous System Health and Disease.Biomolecules · 2025Review
- Lactylation in ischemic brain injury-metabolic mechanisms, neuroinflammation, and therapeutic targets: A review.Biomolecules & biomedicine · 2025Review
- Lactylation Modification and Aging: A Molecular Link in the Life Process.Aging and disease · 2025Review
- Lactylation: A Novel Epigenetic Regulator of Cellular Senescence.Aging and disease · 2025Review
- Gastrodin attenuates rheumatoid arthritis by targeting KAT8 to inhibit the lactylation of H3K9.Frontiers in pharmacology · 2025Article
- Lactate-induced lactylation: from basic research to clinical perspectives.Frontiers in pharmacology · 2025Review
- Histone Lactylation in Diseases: Regulation by Traditional Chinese Medicine and Therapeutic Implications.Drug design, development and therapy · 2025Review
- Lactylation in post-stroke fatigue: linking metabolic dysregulation to neuroinflammation.Frontiers in neuroscience · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
backgroundHypoxia-induced M1 polarization of microglia and resultant inflammation take part in the damage caused by hypoxic-ischemic encephalopathy (HIE). Histone lactylation, a novel epigenetic modification where lactate is added to lysine residues, may play a role in HIE pathogenesis. This study investigates the role of histone lactylation in hypoxia-induced M1 microglial polarization and inflammation, aiming to provide insights for HIE treatment.
methodsIn this study, we assessed the effects of hypoxia on microglial polarization using both an HIE animal model and an oxygen-glucose deprivation cell model. Histone lactylation at various lysine residues was detected by Western blotting. Microglial polarization and inflammatory cytokines were analyzed by immunofluorescence, qPCR, and Western blotting. RNA sequencing, ChIP-qPCR, and siRNA were used to elucidate mechanisms of H3K9 lactylation.
resultsH3K9 lactylation increased due to cytoplasmic lactate during M1 polarization. Inhibiting P300 or reducing lactate dehydrogenase A expression decreased H3K9 lactylation, suppressing M1 polarization. Transcriptomic analysis indicated that H3K9 lactylation regulated M1 polarization via the TNF signaling pathway. ChIP-qPCR confirmed H3K9 lactylation enrichment at the TNFα locus, promoting OGD-induced M1 polarization and inflammation.
conclusionsH3K9 lactylation promotes M1 polarization and inflammation via the TNF pathway, identifying it as a potential therapeutic target for neonatal HIE.
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