ArticleJournal of molecular neuroscience : MN2024
Electroacupuncture Alleviates Streptozotocin-Induced Diabetic Neuropathic Pain via the TRPV1-Mediated CaMKII/CREB Pathway in Rats.
Article in Journal of molecular neuroscience : MN, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research trends and insights in acupuncture randomized controlled trials: a bibliometric analysis.Frontiers in medicine · 2026Pooled it
- Crumbling Pathogenesis and Biomarkers for Diabetic Peripheral Neuropathy.Biomedicines · 2025Review
- Rethink of the New Treatment for Refractory Painful Diabetic Peripheral Neuropathy [Response to Letter].Journal of pain research · 2025Article
- Human Umbilical Cord Mesenchymal Stem Cells Ameliorate Diabetic Neuropathic Pain via TRPV1-[CaStem cells international · 2025Article
- Comparative efficacy of moxibustion as an add-on treatment with different durations for diabetic peripheral neuropathy: study protocol for a randomized controlled trial.Frontiers in neurology · 2025Article
- Rethink of the New Treatment for Refractory Painful Diabetic Peripheral Neuropathy [Letter].Journal of pain research · 2025Article
- Article
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Authors and funding
18 authors.
Funding
Abstract
Diabetic neuropathic pain (DNP) is a diabetic complication that causes severe pain and deeply impacts the quality of the sufferer's daily life. Currently, contemporary clinical treatments for DNP generally exhibit a deficiency in effectiveness. Electroacupuncture (EA) is recognized as a highly effective and safe treatment for DNP with few side effects. Regrettably, the processes via which EA alleviates DNP are still poorly characterized. Transient receptor potential vanilloid 1 (TRPV1) and phosphorylated calcium/calmodulin-dependent protein kinase II (p-CaMKII) are overexpressed on spinal cord dorsal horn (SCDH) in DNP rats, and co-localization is observed between them. Capsazepine, a TRPV1 antagonist, effectively reduced nociceptive hypersensitivity and downregulated the overexpression of phosphorylated CaMKIIα in rats with DNP. Conversely, the CaMKII inhibitor KN-93 did not have any impact on TRPV1. EA alleviated heightened sensitivity to pain caused by nociceptive stimuli and downregulated the level of TRPV1, p-CaMKIIα, and phosphorylated cyclic adenosine monophosphate response element-binding protein (p-CREB) in DNP rats. Intrathecal injection of capsaicin, on the other hand, reversed the above effects of EA. These findings indicated that the CaMKII/CREB pathway on SCDH is located downstream of TRPV1 and is affected by TRPV1. EA alleviates DNP through the TRPV1-mediated CaMKII/CREB pathway.
Indexed as
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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.