Evidence map›Paper›PMID 31019235›Full record

ArticleScientific reports2019

SMN deficiency causes pain hypersensitivity in a mild SMA mouse model through enhancing excitability of nociceptive dorsal root ganglion neurons.

Ruobing Qu, Fuping Yao, Xiaomin Zhang, Yuan Gao, Tong Liu, Yimin Hua

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 7 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 1 institution in 1 country.

Ruobing QuJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.
Fuping YaoJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.
Xiaomin ZhangJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.
Yuan GaoJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.
Tong LiuJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.ORCID http://orcid.org/0000-0001-9152-5264
Yimin HuaJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China. ymhua@suda.edu.cn.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is a devastating motor neuron degeneration disease caused by a deficiency of the SMN protein. Majority of patients also suffer from chronic pain. However, the pathogenesis of pain in the context of SMA has never been explored. In this study, using various pain tests, we found that a mild SMA mouse model presents with multiple forms of pain hypersensitivity. Patch-clamp recording showed that nociceptive neurons in SMA mouse dorsal root ganglia (DRGs) are hyperexcitable and their sodium current densities are markedly increased. Using quantitative RT-PCR, western blotting and immunofluorescence, we observed enhanced expression of two main voltage-gated sodium channels Na

Indexed as

Disease Models, AnimalAnimalsGanglia, SpinalHumansMice, KnockoutMice, TransgenicMuscular Atrophy, SpinalNAV1.7 Voltage-Gated Sodium ChannelNAV1.8 Voltage-Gated Sodium ChannelNF-kappa BNociceptorsPainPatch-Clamp TechniquesPhosphorylationSurvival of Motor Neuron 1 ProteinNAV1.7 Voltage-Gated Sodium ChannelNAV1.8 Voltage-Gated Sodium ChannelNF-kappa BScn10a protein, mouseScn9a protein, mouseSmn1 protein, mouseSurvival of Motor Neuron 1 Protein

Identifiers

PMID31019235
PMCPMC6482187
OpenAlexW2940706646

What OpenQuestion holds

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Registered trials

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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.