ReviewFrontiers in immunology2022
Neuroinflammation of traumatic brain injury: Roles of extracellular vesicles.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Exploiting blood-based biomarkers to align preclinical models with human traumatic brain injury.Brain : a journal of neurology · 2025Pooled it
- Trial
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Article
- The Dual Roles of Extracellular Vesicle Subtypes in Regulating Traumatic Brain Injury.International journal of molecular sciences · 2026Review
- Extracellular Vesicle and Plasma miRNAs as Candidate Biomarkers of Traumatic Brain Injury in the Context of Polytrauma.International journal of molecular sciences · 2026Article
- Extracellular Vesicles in the Gut-Vascular-Brain Axis: A Missing Mechanistic Link Between IBD and Stroke Risk.Biomolecules · 2026Review
- Hematopoietic cell kinase regulates microglial/macrophage activation to drive neuroinflammation after traumatic brain injury.Cell communication and signaling : CCS · 2026Article
- TNF-mediated hilar interneuron loss and aberrant granule cell migration are associated with chronic cognitive deficits following TBI.Brain, behavior, and immunity · 2026Article
- The Effect of Traumatic Brain Injury on the Gastrointestinal System: A Comprehensive Review.Brain sciences · 2026Review
- Normalization strategies for protein quantification in plasma astrocyte-derived extracellular vesicles: a clinical applicability study.BMC psychiatry · 2026Article
- Unveiling the Proteomic Landscape of Extracellular Vesicles: Implications for Neurodegeneration and Neuroprotection.Journal of neurochemistry · 2026Review
- Modulatory Role of Arbutin on Hepatic Inflammation and Apoptosis After Mild Repetitive Traumatic Brain Injury in Experimental Rats: Involvement of NGF/TrkA and IL-6/JAK2/STAT3 Immune Signaling Crosstalk.Biochemistry research international · 2026Article
- From Falls to Frontal Lobe Dysfunction: A Case Report on the Neurodevelopmental Impact of Pediatric Traumatic Brain Injury.Case reports in psychiatry · 2026Article
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Tuberculous meningitis alters the proteomic landscape of brain-derived extracellular vesicles.bioRxiv : the preprint server for biology · 2025Article
- Brain-Derived Exosomes in Neurodevelopmental and Neuropsychiatric Disorders: Molecular Insights, Therapeutic Potential, and Translational Challenges.Molecular neurobiology · 2025Review
- Daflon attenuates cisplatin-induced cerebellar neurotoxicity, anxiety-like behavior, and motor dysfunction by downregulating TLR4/NF-kB signaling.BMC pharmacology & toxicology · 2025Article
- Purinergic and extracellular vesicle signaling in alcohol-induced blood-brain barrier breakdown and neuroimmune activation.Brain, behavior, and immunity · 2025Review
- Sodium hydrogen sulfide restores HInflammopharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major cause of neurological disorder or death, with a heavy burden on individuals and families. While sustained primary insult leads to damage, subsequent secondary events are considered key pathophysiological characteristics post-TBI, and the inflammatory response is a prominent contributor to the secondary cascade. Neuroinflammation is a multifaceted physiological response and exerts both positive and negative effects on TBI. Extracellular vesicles (EVs), as messengers for intercellular communication, are involved in biological and pathological processes in central nervous system (CNS) diseases and injuries. The number and characteristics of EVs and their cargo in the CNS and peripheral circulation undergo tremendous changes in response to TBI, and these EVs regulate neuroinflammatory reactions by activating prominent receptors on receptor cells or delivering pro- or anti-inflammatory cargo to receptor cells. The purpose of this review is to discuss the possible neuroinflammatory mechanisms of EVs and loading in the context of TBI. Furthermore, we summarize the potential role of diverse types of cell-derived EVs in inflammation following TBI.
Indexed as
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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.