ArticleCNS neuroscience & therapeutics2024
SIRT1 mediates the excitability of spinal CaMKIIα-positive neurons and participates in neuropathic pain by controlling Nav1.3.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sirtuin1 in Spinal Cord Injury: Regulatory Mechanisms, Microenvironment Remodeling and Therapeutic Potential.CNS neuroscience & therapeutics · 2025Pooled it
- Discovery of a novel CaMKⅡα inhibitor by machine learning, molecular docking and molecular dynamics simulation.Journal of computer-aided molecular design · 2026Article
- Modulation of ion channels as emerging therapeutic targets in the treatment of diabetic neuropathy.EXCLI journal · 2026Review
- Pulsed radiofrequency attenuates mechanical hypersensitivity in neuropathic pain rats by activating the Nrf2-regulated CaMKII/NF-κB signaling pathway.The Korean journal of pain · 2026Article
- PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia.Scientific reports · 2025Article
- Article
- 5Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Review
- SIRT1 mediates the excitability of spinal CaMKIIα-positive neurons and participates in neuropathic pain by controlling Nav1.3.CNS neuroscience & therapeutics · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
aimsNeuropathic pain is a common chronic pain disorder, which is largely attributed to spinal central sensitization. Calcium/calmodulin-dependent protein kinase II alpha (CaMKIIα) activation in the spinal dorsal horn (SDH) is a major contributor to spinal sensitization. However, the exact way that CaMKIIα-positive (CaMKIIα
methodsCCI-induced neuropathic pain mice model, Sirt1
resultsThe expression of sodium channel Nav1.3 was increased and the expression of SIRT1 was decreased in the spinal CaMKIIα
conclusionThe findings suggest that an aberrant reduction of spinal SIRT1 after nerve injury epigenetically increases Nav1.3, subsequently activating CaMKIIα
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