Evidence map›Paper›PMID 29533535›Full record

ReviewJournal of diabetes investigation2018

Diabetic neuropathy and the sensory neuron: New aspects of pathogenesis and their treatment implications.

Masaki Kobayashi, Douglas W Zochodne

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
8.3field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
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  7. Article
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  9. Article
  10. Innovative Diabetes Therapies and Impact on Peripheral and Autonomic Diabetic Neuropathies: A State-of-the-Art Review.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2026
    Review
  11. Observational
  12. Review
  13. Desloratadine as the selective 5HTJournal of neuroinflammation · 2025
    Article
  14. Article
  15. Article
  16. Article
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  18. Review
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Masaki KobayashiDepartment of Neurology and Neurological Science, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.ORCID http://orcid.org/0000-0002-5131-1533
Douglas W ZochodneDivision of Neurology and Department of Medicine, Neuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Tokyo Medical and Dental University · JPUniversity of Alberta · CA

Funding

Alberta Heritage Foundation for Medical ResearchAlberta Innovates-Health SolutionsCanadian Diabetes Association OG-3-12-3669Canadian Institutes of Health Research 184584Denyse Lajoie Lake Fellow of the Hotchkiss Brain Institute, Faculty of Medicine, University of CalgaryJuvenile Diabetes FoundationNIH HHS 12GHSU172
6 · The paper itself

Abstract

Diabetic polyneuropathy (DPN) continues to be generally considered as a "microvascular" complication of diabetes mellitus alongside nephropathy and retinopathy. The microvascular hypothesis, however, might be tempered by the concept that diabetes directly targets dorsal root ganglion sensory neurons. This neuron-specific concept, supported by accumulating evidence, might account for important features of DPN, such as its early sensory neuron degeneration. Diabetic sensory neurons develop neuronal atrophy alongside a series of messenger ribonucleic acid (RNA) changes related to declines in structural proteins, increases in heat shock protein, increases in the receptor for advanced glycation end-products, declines in growth factor signaling and other changes. Insulin is recognized as a potent neurotrophic factor, and insulin ligation enhances neurite outgrowth through activation of the phosphoinositide 3-kinase-protein kinase B pathway within sensory neurons and attenuates phenotypic features of experimental DPN. Several interventions, including glucagon-like peptide-1 agonism, and phosphatase and tensin homolog inhibition to activate growth signals in sensory neurons, or heat shock protein overexpression, prevent or reverse neuropathic abnormalities in experimental DPN. Diabetic sensory neurons show a unique pattern of microRNA alterations, a key element of messenger RNA silencing. For example, let-7i is widely expressed in sensory neurons, supports their growth and is depleted in experimental DPN; its replenishment improves features of DPN models. Finally, impairment of pre-messenger RNA splicing in diabetic sensory neurons including abnormal nuclear RNA metabolism and structure with loss of survival motor neuron protein, a neuron survival molecule, and overexpression of CWC22, a splicing factor, offer further novel insights. The present review addresses these new aspects of DPN sensory neurodegeneration.

Indexed as

AnimalsDiabetic NeuropathiesGanglia, SpinalHumansMicrovesselsNerve RegenerationSensory Receptor CellsSignal TransductionDiabetic polyneuropathyNeurodegenerationSensory ganglia

Identifiers

PMID29533535
PMCPMC6215951
OpenAlexW2793396628

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.