ReviewWIREs mechanisms of disease
Astrocyte-mediated mechanisms contribute to traumatic brain injury pathology.
Review in WIREs mechanisms of disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Astrocyte-Microglia Crosstalk in Post-Hemorrhagic Neurovascular Microenvironment: Mechanistic Nodes, Cross-Stroke Comparisons, and Therapeutic Reprogramming.Translational stroke research · 2026Review
- Neuronal Mitochondrial Dysfunction Drives Astrocytic Mitochondrial Transfer after TBI: Reveals the Therapeutic Potential of astrocytic EV-Mito.Research square · 2026Article
- Mechanisms of inflammatory response in secondary brain injury: a review of computational approaches, challenges, and future directions.Biomechanics and modeling in mechanobiology · 2026Review
- SRSF1 as a promising biomarker and key player in the pathogenesis of Alzheimer's disease.Molecular medicine reports · 2026Article
- Preparation and application of modified peach gum polysaccharide in the repair of central nervous system injury.Journal of materials science. Materials in medicine · 2026Article
- GFAP degradation in TBI: linking novel modified products to astrocyte pathology and patient outcome.Acta neuropathologica communications · 2026Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- A single-cell transcriptomic dataset profiling traumatic brain injury and NeuroD1-based gene therapy in mice.Scientific data · 2026Article
- Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics.Scientific reports · 2026Article
- Beyond the Leak: Advanced MRI Assessment of the Blood-Brain Barrier in Neurodegeneration.Neuro-degenerative diseases · 2026Review
- Ultra-high contrast MRI: a new technique for recognizing secondary changes to the brain in patients with persistent symptoms following traumatic brain injury.Neuroradiology · 2026Article
- Sex differences in neurobehavior and the adult hippocampal neurogenic niche: influence of traumatic brain injury and CLIP antagonism.Frontiers in behavioral neuroscience · 2026Article
- Sex hormone dysregulation after traumatic brain injury: interactions with sleep disturbances and seizure susceptibility.Frontiers in neuroscience · 2026Review
- Enduring Effects of Humanin on Mitochondrial Systems in TBI Pathology.Biomolecules · 2025Article
- A study on the establishment of a traumatic brain injury model of tree shrews and the observation of neuroinflammatory responses.IBRO neuroscience reports · 2025Article
- Q Neuron-Induced Hypothermia Promotes Functional Recovery and Suppresses Neuroinflammation after Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A Drug Delivery to Improve Prognosis of Traumatic Brain Injury Mice Through Mouse-Derived Nerve Growth Factor Coated by a Nanoparticle.CNS neuroscience & therapeutics · 2025Article
- Deciphering the Structural Biology of GFAP: Connotations of Its Potency in Presaging the Diagnosis for Traumatic Brain Injury and AD.Neurology international · 2025Review
- Traumatic Brain Injury and Risk of Malignant Brain Tumors in Civilian Populations.JAMA network open · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Astrocytes respond to traumatic brain injury (TBI) with changes to their molecular make-up and cell biology, which results in changes in astrocyte function. These changes can be adaptive, initiating repair processes in the brain, or detrimental, causing secondary damage including neuronal death or abnormal neuronal activity. The response of astrocytes to TBI is often-but not always-accompanied by the upregulation of intermediate filaments, including glial fibrillary acidic protein (GFAP) and vimentin. Because GFAP is often upregulated in the context of nervous system disturbance, reactive astrogliosis is sometimes treated as an "all-or-none" process. However, the extent of astrocytes' cellular, molecular, and physiological adjustments is not equal for each TBI type or even for each astrocyte within the same injured brain. Additionally, new research highlights that different neurological injuries and diseases result in entirely distinctive and sometimes divergent astrocyte changes. Thus, extrapolating findings on astrocyte biology from one pathological context to another is problematic. We summarize the current knowledge about astrocyte responses specific to TBI and point out open questions that the field should tackle to better understand how astrocytes shape TBI outcomes. We address the astrocyte response to focal versus diffuse TBI and heterogeneity of reactive astrocytes within the same brain, the role of intermediate filament upregulation, functional changes to astrocyte function including potassium and glutamate homeostasis, blood-brain barrier maintenance and repair, metabolism, and reactive oxygen species detoxification, sex differences, and factors influencing astrocyte proliferation after TBI. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology.
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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.