Evidence map›Paper›PMID 33371371›Full record

ReviewCells2020

Peripheral Neuropathic Pain: From Experimental Models to Potential Therapeutic Targets in Dorsal Root Ganglion Neurons.

Ti-Yen Yeh, I-Wei Luo, Yu-Lin Hsieh, To-Jung Tseng, Hao Chiang, Sung-Tsang Hsieh

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Ti-Yen YehDepartment of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
I-Wei LuoDepartment of Life Science, College of Life Science, National Taiwan University, Taipei 10617, Taiwan.
Yu-Lin HsiehDepartment of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
To-Jung TsengDepartment of Anatomy, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Hao ChiangAkouos, Inc., Boston, MA 02210, USA.
Sung-Tsang HsiehDepartment of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
National Taiwan University · TWChung Shan Medical University · TWKaohsiung Medical University · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain exerts a global burden caused by the lesions in the somatosensory nerve system, including the central and peripheral nervous systems. The mechanisms of nerve injury-induced neuropathic pain involve multiple mechanisms, various signaling pathways, and molecules. Currently, poor efficacy is the major limitation of medications for treating neuropathic pain. Thus, understanding the detailed molecular mechanisms should shed light on the development of new therapeutic strategies for neuropathic pain. Several well-established in vivo pain models were used to investigate the detail mechanisms of peripheral neuropathic pain. Molecular mediators of pain are regulated differentially in various forms of neuropathic pain models; these regulators include purinergic receptors, transient receptor potential receptor channels, and voltage-gated sodium and calcium channels. Meanwhile, post-translational modification and transcriptional regulation are also altered in these pain models and have been reported to mediate several pain related molecules. In this review, we focus on molecular mechanisms and mediators of neuropathic pain with their corresponding transcriptional regulation and post-translational modification underlying peripheral sensitization in the dorsal root ganglia. Taken together, these molecular mediators and their modification and regulations provide excellent targets for neuropathic pain treatment.

Indexed as

Gene Expression RegulationAcrylamideAnimalsDiterpenesExtracellular Signal-Regulated MAP KinasesGanglia, SpinalGuidelines as TopicHumansNeuralgiaNeuronsProtein Processing, Post-TranslationalSpinal CordSpinal NervesVoltage-Gated Sodium ChannelsAcrylamideDiterpenesExtracellular Signal-Regulated MAP KinasesresiniferatoxinVoltage-Gated Sodium Channelsdorsal root ganglianeuropathic painperipheral sensitizationpost-translational modificationtranscriptional regulation

Identifiers

PMID33371371
PMCPMC7767346
OpenAlexW3117556981

What Socratic 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 Socratic graph.