ReviewNeural plasticity2017
The Polarization States of Microglia in TBI: A New Paradigm for Pharmacological Intervention.
Review in Neural plasticity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
71 citing papers in PubMed.
- Serum miR-197-3p as a diagnostic and prognostic biomarker in traumatic brain injury: involvement in MyD88-dependent microglial polarization.Molecular and cellular biochemistry · 2026Article
- M2 microglial exosomal miR-1949 ameliorates sepsis-associated encephalopathy through DKK1/Wnt/β-catenin-mediated microglial repolarization.Archives of pharmacal research · 2026Article
- Head-down position after reperfusion improves cerebral ischaemic injury in rat.Stroke and vascular neurology · 2026Article
- Salvianolic Acid B Inhibits Ferroptosis Through ACSL4 Pathway Regulation in sepsis-associated encephalopathy Mice.Molecular neurobiology · 2026Article
- 3D-bioprinted adipose-derived stem cell-secreted GAS6Journal of nanobiotechnology · 2026Article
- Multi-omics integration reveals TIM-4 as a master regulatory hub of neuroinflammation and neuronal cell death.Frontiers in cell and developmental biology · 2026Article
- LCN2 Regulates Microglia Polarization Through the p38MAPK-PGC-1α-PPARγ Pathway to Alleviate Traumatic Brain Injury.Cell biochemistry and biophysics · 2025Article
- Neurophysiological Markers of Reward Processing Can Inform Preclinical Neurorehabilitation Approaches for Cognitive Impairments Following Brain Injury.Brain sciences · 2025Review
- Single-cell analysis of microglial activation after traumatic brain injury reveals immune signaling pathways linked to mitochondrial dysfunction and brain aging.Frontiers in aging neuroscience · 2025Article
- The immunological landscape of traumatic brain injury: insights from pathophysiology to experimental models.Frontiers in neurology · 2025Review
- Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies.Journal of neuroinflammation · 2024Review
- Abnormal levels of expression of microRNAs in peripheral blood of patients with traumatic brain injury are induced by microglial activation and correlated with severity of injury.European journal of medical research · 2024Article
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- The Rehabilitation Potential of Neurostimulation for Mild Traumatic Brain Injury in Animal and Human Studies.Brain sciences · 2023Review
- Single Versus Repetitive Traumatic Brain Injury: Current Knowledge on the Chronic Outcomes, Neuropathology and the Role of TDP-43 Proteinopathy.Experimental neurobiology · 2023Review
- Inhibition of P2X4 and P2X7 receptors improves histological and behavioral outcomes after experimental traumatic brain injury in rats.Experimental and therapeutic medicine · 2023Article
- Mini-Review: Role of Drugs Affecting Renin-Angiotensin System (RAS) in Traumatic Brain Injury (TBI): What We Know and What We Should Know.Korean journal of neurotrauma · 2023Review
- Review
- Review
- Microglial-oligodendrocyte interactions in myelination and neurological function recovery after traumatic brain injury.Journal of neuroinflammation · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a serious medical and social problem worldwide. Because of the complex pathophysiological mechanisms of TBI, effective pharmacotherapy is still lacking. The microglial cells are resident tissue macrophages located in the brain and have two major polarization states, M1 phenotype and M2 phenotype, when activated. The M1 phenotype is related to the release of proinflammatory cytokines and secondary brain injury, while the M2 phenotype has been proved to be responsible for the release of anti-inflammation cytokines and for central nervous system (CNS) repair. In animal models, pharmacological strategies inhibiting the M1 phenotype and promoting the M2 phenotype of microglial cells could alleviate cerebral damage and improve neurological function recovery after TBI. In this review, we aimed to summarize the current knowledge about the pathological significance of microglial M1/M2 polarization in the pathophysiology of TBI. In addition, we reviewed several drugs that have provided neuroprotective effects against brain injury following TBI by altering the polarization states of the microglia. We emphasized that future investigation of the regulation mechanisms of microglial M1/M2 polarization in TBI is anticipated, which could contribute to the development of new targets of pharmacological intervention in TBI.
Indexed as
Identifiers
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.