ArticleThe Korean journal of pain2023
Antisense oligodeoxynucleotides against dynamin-related protein 1 reduce remifentanil-induced hyperalgesia by modulating spinal N-methyl-D-aspartate receptor expression in rats.
Article in The Korean journal of pain, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Pooled it
- Voltage-gated sodium channel 1.8 contributes to hyperalgesia induced by the coexistence of anxiety and remifentanil exposure.The Korean journal of pain · 2026Article
- Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling.Journal of pain research · 2026Article
- Effects of different anesthetics on remifentanil-induced postinfusion hyperalgesia in patients undergoing percutaneous endoscopic interlaminar discectomy: a randomized controlled trial.Frontiers in medicine · 2025Article
- Targeting the Main Sources of Reactive Oxygen Species Production: Possible Therapeutic Implications in Chronic Pain.Current neuropharmacology · 2024Review
- Towards precision pain management-the case for targeting DRP1 in remifentanil-induced hyperalgesia.The Korean journal of pain · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Spinal N-methyl-D-aspartate (NMDA) receptor activation is attributed to remifentanil-induced hyperalgesia (RIH). However, the specific mechanism and subsequent treatment is still unknown. Previous studies have shown that the dynamin-related protein 1 (DRP1)-mitochondria-reactive oxygen species (ROS) pathway plays an important role in neuropathic pain. This study examined whether antisense oligodeoxynucleotides against DRP1 (AS-DRP1) could reverse RIH. Methods: The authors first measured changes in paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) at 24 hours before remifentanil infusion and 4, 8, 24, and 48 hours after infusion. The expression levels of DRP1 and NR Results: After remifentanil exposure, upregulation of spinal DRP1 and NR Conclusions: These results indicate that AS-DRP1 could modulate NMDA receptor expression to prevent RIH through the DRP1-mitochondria-ROS pathway.
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