Evidence map›Paper›PMID 29806529›Full record

ArticleMolecular pain

HCN2 contributes to oxaliplatin-induced neuropathic pain through activation of the CaMKII/CREB cascade in spinal neurons.

Xiaoyu Liu, Lidong Zhang, Li Jin, Yuanhui Tan, Weiyan Li, Jun Tang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Oxaliplatin-induced peripheral neuropathy: from pathogenesis to treatment.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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  11. CREB Participates in Paclitaxel-Induced Neuropathic Pain Genesis Through Transcriptional Activation of Dnmt3a in Primary Sensory Neurons.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
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  16. An integrated review on new targets in the treatment of neuropathic pain.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Xiaoyu Liu1 Department of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China.
Lidong Zhang1 Department of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China.
Li Jin1 Department of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China.
Yuanhui Tan1 Department of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China.
Weiyan Li1 Department of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China.
Jun Tang1 Department of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China.
Nanjing University · CNNanjing General Hospital of Nanjing Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence showed that hyperpolarization-activated cation channels (HCN) participate in the development of inflammatory and neuropathic pain. However, the role of HCN2 in oxaliplatin-induced neuropathic pain remains unknown. Here, we found that HCN2 expression was upregulated in a rat model of oxaliplatin-induced neuropathic pain. Intrathecal injection of ZD7288, an HCN specific inhibitor, decreased the HCN2 level, as well as weakened the neuropathic pain behaviors compared to naive rats. Besides, mechanistic studies revealed that the expression of the spinal N-methyl-D-aspartate receptor subunit 2B was increased after oxaliplatin administration and was reduced by ZD7288 administration. The nociceptive behaviors were reversed by NR2B antagonist Ro 25-6981 in HCN2-overexpression rats. Furthermore, the underlying cellular mechanism demonstrated that ZD7288 administration restrained the enhanced activation of the neuronal calcium-calmodulin-dependent kinase II (CaMKII)/cyclic adenosine monophosphate response element-binding protein cascade after oxaliplatin administration. Moreover, pretreatment of CaMKII inhibitor KN-93 suppressed the nociceptive behaviors, as well as NR2B upregulation induced by overexpression of HCN2. In a word, HCN2 is conducive to oxaliplatin-induced neuropathic pain by activating the neuronal CaMKII/CREB cascade.

Indexed as

AnimalsBehavior, AnimalCalcium-Calmodulin-Dependent Protein Kinase Type 2Cyclic AMP Response Element-Binding ProteinDisease Models, AnimalHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMaleNeuralgiaNeuronsOrganoplatinum CompoundsOxaliplatinPotassium ChannelsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSignal TransductionSpinal CordCalcium-Calmodulin-Dependent Protein Kinase Type 2Cyclic AMP Response Element-Binding ProteinHcn2 protein, ratHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsNR2B NMDA receptorOrganoplatinum CompoundsOxaliplatinPotassium ChannelsReceptors, N-Methyl-D-AspartateCaMKII/CREBHCN2neuropathic painNR2Boxaliplatin

Identifiers

PMID29806529
PMCPMC5974562
OpenAlexW2807137298

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.