ArticleCell death discovery2022
microRNA-140-3p protects hippocampal neuron against pyroptosis to attenuate sevoflurane inhalation-induced post-operative cognitive dysfunction in rats via activation of HTR2A/ERK/Nrf2 axis by targeting DNMT1.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Mechanism of miR-140-3p reducing anesthesia induced neurotoxicity by downregulating BACE1 expression.Journal of neurovirology · 2026Article
- Mitophagy in perioperative neurocognitive disorder: mechanisms and therapeutic strategies.European journal of medical research · 2025Review
- Human dental follicle stem cell-derived exosomes reduce root resorption by inhibiting periodontal ligament cell pyroptosis.Stem cell research & therapy · 2025Article
- lncRNA PART1 improves sevoflurane-induced impairments in learning and cognitive function by regulating miR-16-5p expression and reducing neuroinflammation.Toxicology research · 2025Article
- Bibliometric Analysis of Neuroinflammation and Postoperative Cognitive Dysfunction.Brain and behavior · 2025Article
- The role of sevoflurane in postoperative cognitive dysfunction.Medical gas research · 2024Article
- Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity.Cell biology and toxicology · 2024Review
- Sevoflurane augments neuroinflammation by regulating DUSP6 via YTHDF1 in postoperative cognitive dysfunction.Toxicology research · 2024Article
- MSC-derived exosomal miR-140-3p improves cognitive dysfunction in sepsis-associated encephalopathy by HMGB1 and S-lactoylglutathione metabolism.Communications biology · 2024Article
- Article
- mtDNA-cGAS-STING axis-dependent NLRP3 inflammasome activation contributes to postoperative cognitive dysfunction induced by sevoflurane in mice.International journal of biological sciences · 2024Article
- Research Advances of Mitochondrial Dysfunction in Perioperative Neurocognitive Disorders.Neurochemical research · 2023Review
- Novel Mechanisms of Perioperative Neurocognitive Disorders: Ferroptosis and Pyroptosis.Neurochemical research · 2023Review
- Dexmedetomidine attenuates neuroinflammation and microglia activation in LPS-stimulated BV2 microglia cells through targeting circ-Shank3/miR-140-3p/TLR4 axis.European journal of histochemistry : EJH · 2023Article
- Hypoxic preconditioned mesenchymal stem cells ameliorate rat brain injury after cardiopulmonary resuscitation by suppressing neuronal pyroptosis.Journal of cellular and molecular medicine · 2023Article
- The Expression Levels of MicroRNAs Differentially Expressed in Sudden Sensorineural Hearing Loss Patients' Serum Are Unchanged for up to 12 Months after Hearing Loss Onset.International journal of molecular sciences · 2023Article
- The role of pyroptosis in cognitive impairment.Frontiers in neuroscience · 2023Review
- The NLRP3 inflammasome is a potential mechanism and therapeutic target for perioperative neurocognitive disorders.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of post-operative cognitive dysfunction (POCD) remains a relatively prevalent complication in the elderly after surgery, especially in those receiving sevoflurane (Sevo) anesthesia. microRNA (miR)-140-3p has been demonstrated to orchestrate neuroinflammation and neuron apoptosis. However, the role of miR-140-3p in POCD remains largely unknown. In this context, this research was designed to explore whether miR-140-3p mediated Sevo inhalation-induced POCD in rats. A POCD rat model was established by Sevo inhalation, and a Sevo cell model was constructed in primary hippocampal neurons isolated from rats, followed by detection of miR-140-30 and HTR2A expression. Then, gain- and loss-of-function assays were implemented in rats and neurons. In rats, the cognitive function was evaluated by Water maze test and step-through test, and neuron apoptosis by TUNEL staining. In neurons, cell viability, apoptosis, and pyroptosis-related factors were tested by MTT, flow cytometry, and Western blot analysis respectively. Interaction between HTR2A and DNMT1 was assessed by MSP, and ChIP assay, and interaction between miR-140-3p and DNMT1 by dual-luciferase reporter assay, RIP and RNA pull-down. HTR2A and miR-140-3p were downregulated in POCD rats and Sevo-treated hippocampal neurons. Mechanistically, miR-140-3p negatively targeted DNMT1 to decrease HTR2A promoter methylation, thus upregulation HTR2A to activate ERK/Nrf2 pathway. miR-140-3p or HTR2A overexpression or activation of ERK/Nrf2 pathway elevated neuron viability and diminished their apoptosis and pyroptosis while alleviating Sevo-induced POCD in rats. Collectively, miR-140-3p might repress neuron pyroptosis to alleviate Sevo inhalation-induced POCD in rats via DNMT1/HTR2A/ERK/Nrf2 axis.
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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.