Evidence map›Paper›PMID 28250049›Full record

ArticleDisease models & mechanisms2017

Diabetic polyneuropathy, sensory neurons, nuclear structure and spliceosome alterations: a role for CWC22.

Masaki Kobayashi, Ambika Chandrasekhar, Chu Cheng, Jose A Martinez, Hilarie Ng, Cristiane de la Hoz, Douglas W Zochodne

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Diabetic neuropathy: cutting-edge research and future directions.Signal transduction and targeted therapy · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Metabolic Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Diabetic neuropathy.Nature reviews. Disease primers · 2019
    Article
  19. Review
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 2 institutions in 1 country.

Masaki KobayashiDivision of Neurology and Department of Medicine, Faculty of Medicine and Dentistry, and the Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada, T6G 2G3.
Ambika ChandrasekharDivision of Neurology and Department of Medicine, Faculty of Medicine and Dentistry, and the Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada, T6G 2G3.
Chu ChengHotchkiss Brain Institute and Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Canada, T2N 4N1.
Jose A MartinezHotchkiss Brain Institute and Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Canada, T2N 4N1.
Hilarie NgHotchkiss Brain Institute and Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Canada, T2N 4N1.
Cristiane de la HozHotchkiss Brain Institute and Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Canada, T2N 4N1.
Douglas W ZochodneDivision of Neurology and Department of Medicine, Faculty of Medicine and Dentistry, and the Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada, T6G 2G3 zochodne@ualberta.ca.ORCID 0000-0003-1692-5983
University of Calgary · CAUniversity of Alberta · CA

Funding

CIHR FRN184584
6 · The paper itself

Abstract

Unique deficits in the function of adult sensory neurons as part of their early neurodegeneration might account for progressive polyneuropathy during chronic diabetes mellitus. Here, we provide structural and functional evidence for aberrant pre-mRNA splicing in a chronic type 1 model of experimental diabetic polyneuropathy (DPN). Cajal bodies (CBs), unique nuclear substructures involved in RNA splicing, increased in number in diabetic sensory neurons, but their expected colocalization with survival motor neuron (SMN) proteins was reduced - a mislocalization described in motor neurons of spinal muscular atrophy. Small nuclear ribonucleoprotein particles (snRNPs), also participants in the spliceosome, had abnormal multiple nuclear foci unassociated with CBs, and their associated snRNAs were reduced. CWC22, a key spliceosome protein, was aberrantly upregulated in diabetic dorsal root ganglia (DRG), and impaired neuronal function. CWC22 attenuated sensory neuron plasticity, with knockdown

Indexed as

AnimalsAtrophyCell NucleusCoiled BodiesDiabetes Mellitus, ExperimentalDiabetic NeuropathiesGanglia, SpinalGene Knockdown TechniquesMice, Inbred C57BLNeural ConductionNeuronal OutgrowthNuclear ProteinsRibonucleoproteins, Small NuclearRNA-Binding ProteinsRNA, Small InterferingRNA, Small NuclearCWC22 protein, mouseNuclear ProteinsRibonucleoproteins, Small NuclearRNA-Binding ProteinsRNA, Small InterferingRNA, Small NuclearSMN Complex ProteinsDiabetic polyneuropathyGemini of coiled bodiesSensory gangliaSmall nuclear ribonucleoproteinsSMN complex proteins

Identifiers

PMID28250049
PMCPMC5374325
OpenAlexW2592910549

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.