ArticleJournal of neuroinflammation2025
TREM2 affects DAM-like cell transformation in the acute phase of TBI in mice by regulating microglial glycolysis.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- A Unified Framework for Spinal Cord Injury Repair: Metabolic-Nutritional Microenvironment Remodeling, Immune Modulation, and Neural Regeneration.Molecular neurobiology · 2026Review
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.Clinical and translational medicine · 2026Article
- Innate immune crosstalk in ALS/FTD pathogenesis.Cell insight · 2026Review
- Metabolic Reprogramming of Brain Microglia: Implications for Aging and Aging-Associated Neurodegenerative Diseases.Aging cell · 2026Review
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
- Remote Ischemic Postconditioning Attenuates Neuroinflammation and Suggests a Potential Benefit for Early Neurological Recovery after Subarachnoid Hemorrhage via the IL-9/JAK2-STAT5 Signaling Pathway.Translational stroke research · 2026Article
- 1-deoxysphinganine promoted microglial glycolytic reprogramming and neuroinflammation in alzheimer's disease.Translational psychiatry · 2026Article
- Therapeutic Targeting of Microglial Hexokinase-2 Recalibrates Inflammasome Activation and Improves Functional Recovery After Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- TREM2 Facilitates Myelin Debris Clearance but Exacerbates Chronic Inflammation and Fibrosis After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Revisiting TREM2: from multi-omics signaling networks to clinical translation.Frontiers in immunology · 2026Review
- Inhibition of astrocyte signaling leads to sex-specific changes in microglia phenotypes in a diet-based model of cerebral small vessel disease.Journal of neuroinflammation · 2025Article
- Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research.Molecular neurodegeneration · 2025Review
- Astrocytic and microglial cell functions in neuroinflammatory diseases and their animal models.Frontiers in cellular neuroscience · 2025Review
- The dual role of microglia in Alzheimer's disease: from immune regulation to pathological progression.Frontiers in aging neuroscience · 2025Review
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13 authors.
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Abstract
backgroundTraumatic brain injury (TBI) is characterized by high mortality and disability rates. Disease-associated microglia (DAM) are a newly discovered subtype of microglia. However, their presence and function in the acute phase of TBI remain unclear. Although glycolysis is important for microglial differentiation, its regulatory role in DAM transformation during the acute phase of TBI is still unclear. In this study, we investigated the functions of DAM-like cells in the acute phase of TBI in mice, as well as the relationship between their transformation and glycolysis.
methodsIn this study, a controlled cortical impact model was used to induce TBI in adult male wild-type (WT) C57BL/6 mice and adult male TREM2 knockout mice. Various techniques were used to assess the role of DAM-like cells in TBI and the effects of glycolysis on DAM-like cells, including RT‒qPCR, immunofluorescence assays, behavioural tests, extracellular acidification rate (ECAR) tests, Western blot analysis, cell magnetic sorting and culture, glucose and lactate assays, and flow cytometry.
resultsDAM-like cells were observed in the acute phase of TBI in mice, and their transformation depended on TREM2 expression. TREM2 knockout impaired neurological recovery in TBI mice, possibly due in part to their role in clearing debris and secreting VEGFa and BDNF. Moreover, DAM-like cells exhibited significantly increased glycolytic activity. TREM2 regulated the AKT‒mTOR‒HIF-1α pathway and glycolysis in microglia in the acute phase of TBI. The increase in glycolysis in microglia partially contributed to the transformation of DAM-like cells in the acute phase of TBI in mice.
conclusionsTaken together, the results of our study demonstrated that DAM-like cells were present in the acute phase of TBI in mice. TREM2 might influence DAM-like cell transformation by modulating the glycolysis of microglia. Our results provide a new possible pathway for intervening TBI.
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