Evidence map›Paper›PMID 32354292›Full record

ArticleMolecular pain

Wnt/

Xinxin Zhou, Lei Tao, Mengru Zhao, Shengjun Wu, Enoch Obeng, Dan Wang, Wenping Zhang

Open access · goldAbstract read
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 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
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

7 authors at 3 institutions in 1 country.

Xinxin ZhouZhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Science and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.
Lei TaoSchool of Life Sciences, East China Normal University, Shanghai, China.
Mengru ZhaoZhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Science and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.
Shengjun WuClinical Laboratory of Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Enoch ObengZhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Science and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.
Dan WangZhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Science and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.
Wenping ZhangZhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Science and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.ORCID 0000-0002-3107-8965
Zhejiang Sci-Tech University · CNEast China Normal University · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV-associated neuropathic pain (HNP) is a common complication for AIDS patients. The pathological mechanism governing HNP has not been elucidated, and HNP has no effective analgesic treatment. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family related to the plasticity of the central nervous system. BDNF dysregulation is involved in many neurological diseases, including neuropathic pain. However, to the best of our knowledge, the role and mechanism of BDNF in HNP have not been elucidated. In this study, we explored this condition in an HNP mouse model induced by intrathecal injection of gp120. We found that Wnt3a and β-catenin expression levels increased in the spinal cord of HNP mice, consequently regulating the expression of BDNF and affecting hypersensitivity. In addition, the blockade of Wing-Int/β-catenin signaling, BDNF/TrkB or the BDNF/p75NTR pathway alleviated mechanical allodynia. BDNF immunoreactivity was colocalized with spinal microglial cells, which were activated in HNP mice. Inhibition of spinal microglial cell activation by minocycline relieved mechanical allodynia in HNP mice. This study helped to elucidate the role of the Wing-Int/β-catenin/BDNF signaling axis in HNP and may establish a foundation for further research investigating the Wing-Int/β-catenin/BDNF signaling axis as a target for HNP treatment.

Indexed as

Wnt Signaling PathwayAnimalsBehavior, AnimalBrain-Derived Neurotrophic FactorHIV Envelope Protein gp120HyperalgesiaInjections, SpinalMice, Inbred ICRMicrogliaModels, BiologicalNeuralgiaNociceptionReceptors, Nerve Growth FactorReceptor, trkBSpinal CordUp-RegulationBrain-Derived Neurotrophic FactorHIV Envelope Protein gp120Ngfr protein, mouseReceptors, Nerve Growth FactorReceptor, trkBbrain-derived neurotrophic factorHIV-associated neuropathic painmicrogliaspinal cordWing-Int

Identifiers

PMID32354292
PMCPMC7227158
OpenAlexW3023966651

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.