Evidence map›Paper›PMID 31934126›Full record

ArticleInternational journal of clinical and experimental pathology2019

Spinal astrocytic FGFR3 activation leads to mechanical hypersensitivity by increased TNF-α in spared nerve injury.

Ke-Yu Xie, Qiang Wang, De-Jun Cao, Jia Liu, Xian-Feng Xie

Open access · greenAbstract read
In one paragraph

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 10 citations in OpenAlex.

  1. Pathogenic Role of FGFR3 Autoantibodies in Small Fiber Neuropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  12. Frontiers in immunology · 2020
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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

5 authors at 2 institutions in 1 country.

Ke-Yu XieAnesthesia Department, Second People's Hospital of Chengdu Chengdu 610017, China.
Qiang WangPathology Department, Navy 971 Hospital of PLA Qingdao 266071, China.
De-Jun CaoAnesthesia Department, Second People's Hospital of Chengdu Chengdu 610017, China.
Jia LiuAnesthesia Department, Second People's Hospital of Chengdu Chengdu 610017, China.
Xian-Feng XieAnesthesia Department, Second People's Hospital of Chengdu Chengdu 610017, China.
Chengdu Second People's Hospital · CNPeople's Liberation Army 401 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulated studies indicated a crucial role of astrocytes in neuropathic pain (NPP) development, spread and potentiation by a communication with the nervous system. Increased GFAP expression in dorsal horn of the spinal cord indicated the participation of astrocyte in NPP. However, the underlying mechanism is still in need of further investigations.

methodsIn our study, the spared nerve injury (SNI) model was established with partial sciatic nerve ligation. The expression status of FGFR3 was studied in spinal dorsal horn of SNI models. The molecular mechanism of spinal astrocytic FGFR3 activation in mechanical hypersensitivity was investigated.

resultsSNI rats showed with hind paw mechanical hypersensitivity and increased GFAP expression in their spinal cords. Increased FGFR3 expression was observed in spinal dorsal horn of SNI models, which was consistent with increased GFAP expression. Elevated FGFR3 upregulates GFAP and TNF-α expression in astrocytes

conclusionFGFR3 is involved in NPP maintenance via FGFR3-TBX3 axis activation induced TNF-α synthesis. FGFR3 and correlated signaling pathways of astrocytes are potential molecular targets for NPP administration.

Indexed as

astrocytefibroblast growth factor receptor-3Neuropathic painTBX3TNF-α

Identifiers

PMID31934126
PMCPMC6949693
OpenAlexW3027177532

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.