ReviewTranslational pediatrics2025
The role of microglia in sepsis-associated encephalopathy: a narrative review.
Review in Translational pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- FPR1 drives sepsis-associated cognitive impairment through region-specific transcriptional and splicing dysregulation in the brain.Metabolic brain disease · 2026Article
- Hippocampal cytopathology orchestrates post-septic cognitive dysfunction.Metabolic brain disease · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objective: Sepsis-associated encephalopathy (SAE) is a severe multifactorial brain dysfunction triggered by severe infections, characterized by neuroinflammation, blood-brain barrier (BBB) breakdown, and persistent neurocognitive deficits. Accumulating evidence indicates that phenotypic polarization of microglia-resident immune cells in the central nervous system (CNS)-plays a central role in SAE pathogenesis. In SAE, microglia exhibit an imbalance in polarization, with sustained pro-inflammatory states and impaired reparative functions, accompanied by activation of the NLRP3 inflammasome, forming a deleterious cycle of neuroinflammation and neuronal damage. This review focuses on three underexplored domains in SAE: neuronal/glial dysfunction, circadian disruption, and gut-brain axis dysregulation. Methods: A systematic literature search was performed in PubMed (1985-2025) using fuzzy-matching mode, with search terms including "microglia", "sepsis-associated encephalopathy", "blood-brain barrier (BBB)", "microglia polarization", "M1/M2 polarization", "NLRP3 inflammasome", "inflammation" "quercetin", and related Medical Subject Headings (MeSH) terms. Key Content and Findings: This review elaborates on the mechanisms underlying neuronal/glial dysfunction, circadian rhythm disruption, and gut-brain axis imbalance in SAE, emphasizing their interactions with microglial polarization and neuroinflammation. Experimental interventions targeting microglial activity (e.g., CSF1R inhibitors) show promise, but complete suppression of microglia is inadvisable due to their essential role in maintaining neural network homeostasis. Conclusions: Future therapeutic strategies for SAE should aim to balance the inhibition of harmful inflammatory responses with the preservation of microglia-mediated reparative processes, while targeting the underexplored domains identified herein to improve neuroprotective efficacy and ultimately translate into tangible clinical benefits for patients.
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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.