Evidence mapPaperPMID 42564001Full record

ReviewFrontiers in endocrinology2026

Mechanisms, translational opportunities for diabetic polyneuropathy.

Honyi Ong, Mingyang Hong, Douglas W Zochodne

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Honyi Ong *Division of Neurology, Department of Medicine, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada.
Mingyang Hong *Division of Neurology, Department of Medicine, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada.
Douglas W ZochodneDivision of Neurology, Department of Medicine, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic polyneuropathy (DPN) is a common complication of types 1 and 2 diabetes mellitus (DM). Peripheral sensory axons are early and primary targets of DPN, rendering sensory loss, pain and impaired quality of life. While several metabolic and other abnormalities, including abnormal insulin signaling and mitochondrial dysfunction contribute toward DPN, effective therapy to reverse or arrest the disorder is not currently available. DPN is a degenerative condition that involves retraction of distal sensory terminals and failure of regenerative repair. This review summarizes current mechanisms of DPN and potential new approaches that may offer translational opportunities for treatment. Many of these targets have yet to be explored in multiple DM models/paradigms and have not yet entered clinical trials. Nonetheless, specific regeneration pathways may offer a future role to encourage sensory axon resilience and regrowth.

Indexed as

Diabetic NeuropathiesTranslational Research, BiomedicalAnimalsAxonsHumansNerve Regenerationaxonal degenerationaxon regenerationdiabetes mellitusdiabetic polyneuropathysensory loss

Identifiers

PMID42564001
PMCPMC13441761

What Socratic 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 Socratic graph.