ReviewBurns & trauma2025
Role of damage-associated molecular patterns in the pathogenesis and therapeutics of traumatic brain injury.
Review in Burns & trauma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Advances in Stereotactic Hematoma Evacuation for Hypertensive Intracerebral Hemorrhage and the Value of Multimodal Monitoring.Cerebrovascular diseases (Basel, Switzerland) · 2026Review
- Meta-inflammation through the lens of macrophage programming and nutrient-sensing ghrelin signaling.Immunometabolism (Cobham, Surrey) · 2026Review
- A Novel Approach to Neuropathic Pain Treatment: Lactylation Targeting Microglia.Molecular neurobiology · 2026Review
- Plasma Lipoproteins as Key Regulators in Neuropathic Pain: A Comprehensive Review of Mechanisms and Clinical Potential.Pain and therapy · 2026Review
- The Potential and Prospects of Hydrogel Applications in Traumatic Brain Injury Treatment.Current issues in molecular biology · 2026Review
- Neuroimmune Mechanisms in Traumatic Brain Injury and Cancer: Parallel Courses or Existence in Different Orbits.Biomedicines · 2026Review
- SIRT1 deacetylates GAPDH to drive microglial glycolysis and neuroinflammation.Frontiers in immunology · 2026Article
- Polyphenol-based modulation of the Glo1-Nrf2-RAGE axis in diabetes and neurodegeneration: mechanistic evidence, translational constraints, and critical appraisal.Frontiers in pharmacology · 2026Review
- Targeting mitofusin 1-mediated mitochondrial dynamics to suppress neuroinflammation and pyroptosis after traumatic brain injury.Burns & trauma · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a serious condition that poses a significant threat to human health globally. It is typically caused by direct trauma to the brain due to external forces such as impact or compression. The progression of TBI occurs in two stages based on physiological and pathological changes: primary and secondary brain injury. During the secondary stage, a large number of damage-associated molecular patterns (DAMPs) are released from injured cells into the extracellular space. These DAMPs trigger or exacerbate pathological conditions, including neuroinflammation, brain edema, diffuse axonal injury, and programmed cell death. The three main types of neural cells-neurons, microglia, and astrocytes-facilitate intercellular communication and functional crosstalk through the release and transmission of DAMPs. This forms the cellular foundation of secondary brain injury pathology. In the later stages of TBI, DAMPs are transported to various organs throughout the body
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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.