Evidence map›Paper›PMID 31765435›Full record

ArticlePloS one2019

Upregulation of ERK phosphorylation in rat dorsal root ganglion neurons contributes to oxaliplatin-induced chronic neuropathic pain.

Toyoaki Maruta, Takayuki Nemoto, Koutaro Hidaka, Tomohiro Koshida, Tetsuro Shirasaka, Toshihiko Yanagita, Ryu Takeya, Isao Tsuneyoshi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-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

25 citing papers in PubMed, 47 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
    Review
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  18. Signaling Pathways in Proton and Non-proton ASIC1a Activation.Frontiers in cellular neuroscience · 2021
    Article
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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

8 authors at 2 institutions in 1 country.

Toyoaki MarutaDepartment of Anesthesiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0002-2660-2179
Takayuki NemotoDepartment of Pharmacology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Koutaro HidakaDepartment of Anesthesiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Tomohiro KoshidaDepartment of Anesthesiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Tetsuro ShirasakaDepartment of Anesthesiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Toshihiko YanagitaDepartment of Clinical Pharmacology, School of Nursing, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Ryu TakeyaDepartment of Pharmacology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Isao TsuneyoshiDepartment of Anesthesiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
University of Miyazaki · JPFukuoka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxaliplatin is the first-line chemotherapy for metastatic colorectal cancer. Unlike other platinum anticancer agents, oxaliplatin does not result in significant renal impairment and ototoxicity. Oxaliplatin, however, has been associated with acute and chronic peripheral neuropathies. Despite the awareness of these side-effects, the underlying mechanisms are yet to be clearly established. Therefore, in this study, we aimed to understand the factors involved in the generation of chronic neuropathy elicited by oxaliplatin treatment. We established a rat model of oxaliplatin-induced neuropathic pain (4 mg kg-1 intraperitoneally). The paw withdrawal thresholds were assessed at different time-points after the treatment, and a significant decrease was observed 3 and 4 weeks after oxaliplatin treatment as compared to the vehicle treatment (4.4 ± 1.0 vs. 16.0 ± 4.1 g; P < 0.05 and 4.4 ± 0.7 vs. 14.8 ± 3.1 g; P < 0.05, respectively). We further evaluated the role of different mitogen-activated protein kinases (MAPKs) pathways in the pathophysiology of neuropathic pain. Although the levels of total extracellular signal-regulated kinase (ERK) 1/2 in the dorsal root ganglia (DRG) were not different between oxaliplatin and vehicle treatment groups, phosphorylated ERK (p-ERK) 1/2 was up-regulated up to 4.5-fold in the oxaliplatin group. Administration of ERK inhibitor PD98059 (6 μg day-1 intrathecally) inhibited oxaliplatin-induced ERK phosphorylation and neuropathic pain. Therefore, upregulation of p-ERK by oxaliplatin in rat DRG and inhibition of mechanical allodynia by an ERK inhibitor in the present study may provide a better understanding of intracellular molecular alterations associated with oxaliplatin-induced neuropathic pain and help in the development of potential therapeutics.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFlavonoidsGanglia, SpinalHyperalgesiaMaleNeuralgiaOxaliplatinPhosphorylationRatsRats, Sprague-DawleyUp-Regulation2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneBrain-Derived Neurotrophic FactorExtracellular Signal-Regulated MAP KinasesFlavonoidsOxaliplatin

Identifiers

PMID31765435
PMCPMC6876879
OpenAlexW2990768607

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.