ReviewBMC anesthesiology2025
Somatostatin and its receptors involvement in sevoflurane-induced neurotoxicity: a narrative review.
Review in BMC anesthesiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Role and mechanism of LINC00662 via targeting let-7 g-5p in sevoflurane-induced cognitive impairment in rats.BMC anesthesiology · 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
14 authors.
Funding
Abstract
As a widely used pediatric anesthetic, sevoflurane presents a paradoxical neurodevelopmental risk during vulnerable brain maturation periods. This review synthesizes emerging evidence on sevoflurane-induced developmental neurotoxicity, with a focus on somatostatin (SST)-SSTR4 signaling and its downstream effects on synaptic integrity. Key findings reveal that sevoflurane exposure disrupts excitatory-inhibitory balance by upregulating hippocampal SST expression, suppressing glutamatergic synaptic markers (vesicular glutamate transporter 1 (vGLUT1), PSD95), and impairing cAMP/PKA signaling-a pathway essential for AMPA receptor trafficking and synaptic plasticity. Mechanistically, SSTR4 activation exacerbates synaptic dysfunction through adenylate cyclase (AC) inhibition, reducing cAMP levels and diminishing AMPA receptor phosphorylation. Primate and rodent models corroborate these effects, linking SST-SSTR4 dysregulation to long-term cognitive deficits. Single-nucleus RNA sequencing in macaques further identifies altered synaptic development genes after sevoflurane exposure. While preclinical data suggest SSTR4 modulation as a therapeutic target, causal relationships between sevoflurane, SSTergic signaling, and synaptic pathology remain unconfirmed. This work underscores the urgency of refining pediatric anesthesia protocols and developing neuroprotective strategies targeting the SST-SSTR4-cAMP/PKA axis. Future research should prioritize spatiotemporal profiling of SST dynamics, validation of SSTR4-specific interventions, and translational studies using non-human primate models to bridge mechanistic insights with clinical outcomes.
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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.