ReviewFrontiers in cellular neuroscience2024
Deplete and repeat: microglial CSF1R inhibition and traumatic brain injury.
Review in Frontiers in cellular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- CD11c + microglia: From basic research to clinical application.Neural regeneration research · 2026Article
- Bridging the gap: neuroinflammation and the dawn of precision medicine in amyotrophic lateral sclerosis.Translational neurodegeneration · 2026Review
- Repeated head impacts establish a senescent cranial bone marrow niche that impairs brain metabolism.Journal of neuroinflammation · 2026Article
- Neuron-derived mitochondrial DNA (mtDNA) activates microglia via the Z-DNA binding protein 1 (ZBP1)-mediated pathway in mild traumatic brain injury.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- BTLA-mediated regulation of neuroimmune responses enhances recovery after intracerebral hemorrhage.Journal of neuroinflammation · 2026Article
- Repeated Mild Head Injury Establishes a Senescent Cranial Bone Marrow Niche that Impairs Brain Metabolism.bioRxiv : the preprint server for biology · 2026Article
- CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Dual immune armies in glaucoma: microglia and monocyte-derived macrophages.Frontiers in immunology · 2026Review
- Microglia depletion improves hippocampal circuit function after mild traumatic brain injury in male mice.Brain, behavior, and immunity · 2026Article
- The senescent niche hypothesis: microglial dysfunction and replacement strategies in drug-resistant epilepsy.Frontiers in immunology · 2026Review
- Identification and validation of microglia-associated genes in ischemic stroke using single-cell and bulk RNA-seq.Molecular brain · 2025Article
- Fate mapping of peripherally-derived macrophages after traumatic brain injury in mice reveals a long-lasting population with a distinct transcriptomic signature.Nature communications · 2025Article
- Intraoperative application of an antioxidant nanoparticle-hydrogel targeting microglia regulates neuroinflammation in traumatic brain injury.Journal of nanobiotechnology · 2025Article
- Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025Review
- Microglial depletion and repopulation differentially modulate sleep and inflammation in a mouse model of traumatic brain injury.Neurobiology of sleep and circadian rhythms · 2025Article
- Diffuse traumatic brain injury induced stimulator of interferons (STING) signaling in microglia drives cortical neuroinflammation, neuronal dysfunction, and impaired cognition.Journal of neuroinflammation · 2025Article
- Synergistic Therapeutic Platform Combining Transcranial Low-Intensity Ultrasound Stimulation and Curcumin Load Liposome Ameliorates Cerebral Ischemia by Modulating Microglia Polarization-Mediated Neuroinflammatory Microenvironment.Research (Washington, D.C.) · 2025Article
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Traumatic brain injury and post-injury sleep fragmentation differentially alter the microglial transcriptome.Frontiers in immunology · 2025Article
- 20-Hydroxyeicosatetraenoic Acid Regulates the Src/EGFR/NF-κB Signaling Pathway Via GPR75 to Activate Microglia and Promote TBI in the Immature Brain.Neurochemical research · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a public health burden affecting millions of people. Sustained neuroinflammation after TBI is often associated with poor outcome. As a result, increased attention has been placed on the role of immune cells in post-injury recovery. Microglia are highly dynamic after TBI and play a key role in the post-injury neuroinflammatory response. Therefore, microglia represent a malleable post-injury target that could substantially influence long-term outcome after TBI. This review highlights the cell specific role of microglia in TBI pathophysiology. Microglia have been manipulated via genetic deletion, drug inhibition, and pharmacological depletion in various pre-clinical TBI models. Notably, colony stimulating factor 1 (CSF1) and its receptor (CSF1R) have gained much traction in recent years as a pharmacological target on microglia. CSF1R is a transmembrane tyrosine kinase receptor that is essential for microglia proliferation, differentiation, and survival. Small molecule inhibitors targeting CSF1R result in a swift and effective depletion of microglia in rodents. Moreover, discontinuation of the inhibitors is sufficient for microglia repopulation. Attention is placed on summarizing studies that incorporate CSF1R inhibition of microglia. Indeed, microglia depletion affects multiple aspects of TBI pathophysiology, including neuroinflammation, oxidative stress, and functional recovery with measurable influence on astrocytes, peripheral immune cells, and neurons. Taken together, the data highlight an important role for microglia in sustaining neuroinflammation and increasing risk of oxidative stress, which lends to neuronal damage and behavioral deficits chronically after TBI. Ultimately, the insights gained from CSF1R depletion of microglia are critical for understanding the temporospatial role that microglia develop in mediating TBI pathophysiology and recovery.
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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.