ReviewCNS neuroscience & therapeutics2026
Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.
Review in CNS neuroscience & therapeutics, 2026. 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.
- ERα Agonist Protects Aged Female Mice From Sevoflurane Neurotoxicity via PTEN Nuclear Translocation.CNS neuroscience & therapeutics · 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
3 authors.
Funding
Abstract
backgroundPostoperative cognitive dysfunction (POCD) is an increasingly recognized neurological complication following surgery, particularly in elderly patients. It significantly hinders recovery and impairs the quality of life. Sevoflurane, a commonly used volatile anesthetic, has been implicated in enhancing the incidence and severity of POCD. At the molecular level, synaptic dysfunction is a major contributor to cognitive decline associated with POCD. Recent studies have highlighted ferroptosis, an iron-dependent form of cell death driven by lipid peroxidation, as a critical mechanism behind synaptic damage and cognitive decline.
methodsThis review synthesizes current research on the role of ferroptosis in POCD, focusing on its impact on synaptic dysfunction. We also explore the potential of nanomedicine, particularly intelligent responsive nanodrug delivery systems, in targeting ferroptotic pathways. These nanoplatforms, with their high brain delivery efficiency and specificity, have been shown to modulate ferroptosis signaling and reduce neuronal injury, thereby potentially promoting cognitive recovery.
resultsFerroptosis plays a significant role in exacerbating cognitive deficits by disrupting synaptic membranes and mitochondria, which contribute to synaptic dysfunction. Emerging evidence suggests that interventions targeting ferroptosis pathways can mitigate these effects, offering a novel therapeutic avenue for POCD. Nanomedicine approaches, especially those utilizing responsive nanodrug delivery systems, have shown promise in effectively targeting ferroptotic pathways with high specificity, leading to reductions in synaptic injury and enhanced cognitive recovery.
conclusionFerroptosis is a key mechanism driving synaptic dysfunction and cognitive decline in POCD. Targeting ferroptotic pathways using nanomedicine-based strategies holds considerable promise for mitigating POCD and promoting cognitive recovery. Further research is needed to optimize these therapeutic approaches for clinical application in POCD management.
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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 Socratic graph.