ArticleInternational journal of clinical and experimental pathology2019
Decreased HCN2 channel expression attenuates neuropathic pain by inhibiting pro-inflammatory reactions and NF-κB activation in mice.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.Neuroscience bulletin · 2025Review
- Amelioration of Chemotherapy Induced Neuropathic Pain using Novel Nicotinic Acid Derivatives with possible HCN channel binding ability.Molecular neurobiology · 2025Article
- Ion Channel Genes in Painful Neuropathies.Biomedicines · 2023Review
- Stretch-Induced Down-Regulation of HCN2 Suppresses Contractile Activity.Molecules (Basel, Switzerland) · 2023Article
- Up-regulation of HCN2 channels in a thalamocortical circuit mediates allodynia in mice.National science review · 2023Article
- Bibliometric analysis of hyperpolarization-activated cyclic nucleotide-gated (HCN)channels research (2004-2020).Channels (Austin, Tex.) · 2022Article
- Changes in peripheral HCN2 channels during persistent inflammation.Channels (Austin, Tex.) · 2021Article
- P2X3 receptors contribute to transition from acute to chronic muscle pain.Purinergic signalling · 2020Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2) ion channel activity plays a crucial role in the progress of peripheral neuropathic pain (PNP). However, the mechanism of HCN2 channels on PNP remains unclear. Here, we investigated the effects of HCN2 channel expression on the mechanical allodynia and thermal hyperalgesia, the local inflammatory response, the activation of astrocytes, microglia and transcription factor NF-κB in mice with spared sciatic nerve injury (SNI). The present study showed that the expression of HCN2 channels was increased in L4-L5 ipsilateral spinal dorsal horns, accompanied by a decreased paw mechanical withdrawal threshold (MWT) and paw withdrawal latency (PWL) in SNI mice. After intrathecal injection of ZD-7288 and si-HCN2, both MWT and PWL were significantly increased, while the level of pro-inflammatory factors TNF-α, IL-1β and MCP-1 were decreased in L4-L5 ipsilateral spinal dorsal horn. Furthermore, the inhibition of HCN2 channels reduces the activated astrocytes and microglia, and suppressed NF-κB p65 activation and nuclear translocation. In conclusion, the present study suggests that decreased HCN2 channel expression attenuates neuropathic pain by inhibiting pro-inflammatory reactions and NF-κB activation.
Indexed as
Identifiers
31933729PMC6944015W3006247028What OpenQuestion holds
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.