ArticleJournal of neurochemistry2020
Involvement of homodomain interacting protein kinase 2-c-Jun N-terminal kinase/c-Jun cascade in the long-term synaptic toxicity and cognition impairment induced by neonatal Sevoflurane exposure.
Article in Journal of neurochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Neonatal sevoflurane exposure disrupts the lung-brain axis and drives microglial neuroinflammation and cognitive deficits.Journal of neuroinflammation · 2026Article
- Transcriptomic Changes Associated with Electroacupuncture in a DMCAO Model of Delayed Cognitive Impairment.Current neurovascular research · 2026Article
- MANF improves cognitive function and attenuates neuroinflammation in APP/PS1 transgenic mice through the TLR4/MYD88/NF-κB signaling pathway.Journal of anesthesia and translational medicine · 2025Article
- JNK inhibition mitigates sepsis-associated encephalopathy via attenuation of neuroinflammation, oxidative stress and apoptosis.Metabolic brain disease · 2025Article
- Integrated ribosome and proteome analyses reveal insights into sevoflurane-induced long-term social behavior and cognitive dysfunctions through ADNP inhibition in neonatal mice.Zoological research · 2024Article
- Complement C1q-mediated microglial synaptic elimination by enhancing desialylation underlies sevoflurane-induced developmental neurotoxicity.Cell & bioscience · 2024Article
- SynCAM1 deficiency in the hippocampal parvalbumin interneurons contributes to sevoflurane-induced cognitive impairment in neonatal rats.CNS neuroscience & therapeutics · 2024Article
- Ketamine counteracts sevoflurane-induced depressive-like behavior and synaptic plasticity impairments through the adenosine A2A receptor/ERK pathway in rats.Molecular neurobiology · 2023Article
- HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Sevoflurane-Induced Neurotoxicity in the Developing Hippocampus via HIPK2/AKT/mTOR Signaling.Neurotoxicity research · 2022Article
- Research progress on molecular mechanisms of general anesthetic-induced neurotoxicity and cognitive impairment in the developing brain.Frontiers in neurology · 2022Review
- Decoding competitive endogenous RNA regulatory network in postoperative cognitive dysfunction.Frontiers in neuroscience · 2022Article
- Effects of General Anesthetics on Synaptic Transmission and Plasticity.Current neuropharmacology · 2022Review
- Melatonin pretreatment alleviates the long-term synaptic toxicity and dysmyelination induced by neonatal Sevoflurane exposure via MT1 receptor-mediated Wnt signaling modulation.Journal of pineal research · 2021Article
- Early-Life Multiple Sevoflurane Exposures Alleviate Long-term Anxiety-Like Behaviors in Mice via the proBDNF/ERK Pathway.Molecular neurobiology · 2021Article
- The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer's Disease in APPSwe/PS1dE9 Mice.Frontiers in molecular neuroscience · 2020Article
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10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Sevoflurane is one of the most widely used anesthetics with recent concerns rising about its pediatric application. The synaptic toxicity and mechanisms underlying its long-term cognition impairment remain unclear. In this study, we investigated the expression and roles of homeodomain interacting protein kinase 2 (HIPK2), a stress activating kinase involved in neuronal survival and synaptic plasticity, and its downstream c-Jun N-terminal kinase (JNK)/c-Jun signaling in the long-term toxicity of neonatal Sevoflurane exposure. Our data showed that neonatal Sevoflurane exposure results in impairment of memory, enhancement of anxiety, less number of excitatory synapses and lower levels of synaptic proteins in the hippocampus of adult rats without significant changes of hippocampal neuron numbers. Up-regulation of HIPK2 and JNK/c-Jun was observed in hippocampal granular neurons shortly after Sevoflurane exposure and persisted to adult. 5-((6-Oxo-5-(6-(piperazin-1-yl)pyridin-3-yl)-1,6-dihydropyridin-3-yl)methylene)thiazolidine-2,4-dione trifluoroacetate, antagonist of HIPK2, could significantly rescue the cognition impairment, decrease in long-term potentiation, reduction in spine density and activation of JNK/c-Jun induced by Sevoflurane. JNK antagonist SP600125 partially restored synapse development and cognitive function without affecting the expression of HIPK2. These data, in together, revealed a novel role of HIPK2-JNK/c-Jun signaling in the long-term synaptic toxicity and cognition impairment of neonatal Sevoflurane exposure, indicating HIPK2-JNK/c-Jun cascade as a potential target for reducing the synaptic toxicity of Sevoflurane. Cover Image for this issue: doi: 10.1111/jnc.14757.
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