ArticleClinical and translational medicine2026
ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundTraumatic brain injury (TBI) is a leading cause of death and long-term disability worldwide. Secondary cerebral oedema, driven by neuroinflammation and blood-brain barrier (BBB) disruption, critically determines poor outcomes, yet effective targeted therapies remain absent. This study aimed to identify immune cell subsets associated with post-TBI cerebral oedema and to explore their functional contributions in preclinical models.
methodsWe integrated single-cell transcriptomic datasets from a mouse TBI model (GSE175430) and human intracerebral haemorrhage (ICH) perihaematomal oedema samples (GSE266873) with our previously published temporal bulk RNA-seq profiling data. Through cross-species comparative analysis, Mfuzz clustering, AUCell scoring and gene set enrichment analysis (GSEA), Acp5 was identified as an oedema-associated signature gene, and its macrophage-enriched expression pattern was supported by single-cell profiling and immunofluorescence colocalisation. Using the controlled cortical impact (CCI) model, we validated Acp5 expression dynamics across injury severities. Pharmacological inhibition (AubipyOMe) and genetic knockout of Acp5 were employed to assess brain oedema, neuroinflammation, neurological function and long-term cognitive recovery.
resultsA previously unrecognised population of ACP5-positive monocytes/macrophages infiltrated the brain parenchyma within 1-3 days post-injury, coinciding with peak oedema severity and neurological deficits. Inhibiting ACP5 significantly reduced brain water content, BBB leakage and proinflammatory cytokines, while improving sensorimotor function. Mechanistically, ACP5-positive macrophages were associated with CSF2-related JAK/STAT and NF-κB signalling. Genetic Acp5 ablation attenuated acute macrophage infiltration and neuroinflammation, and was associated with improved long-term behavioural outcomes.
conclusionsACP5-positive macrophages represent an injury-associated myeloid population that contributes to neuroinflammatory and oedema-related phenotypes after experimental TBI. Pharmacological and genetic findings provide preclinical evidence supporting further investigation of ACP5 and CSF2-related signalling in secondary TBI injury.
Indexed as
Identifiers
What Socratic 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 Socratic graph.