Evidence map›Paper›PMID 26025657›Full record

ArticleActa neuropathologica2015

Dysregulated IGFBP5 expression causes axon degeneration and motoneuron loss in diabetic neuropathy.

Christian M Simon, Stefanie Rauskolb, Jennifer M Gunnersen, Bettina Holtmann, Carsten Drepper, Benjamin Dombert, Massimiliano Braga, Stefan Wiese, Sibylle Jablonka, Dirk Pühringer and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Sonic Hedgehog Agonists Induce Repair Schwann Cells.Biotechnology and bioengineering · 2025
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  4. Review
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  12. IGFBP5 Promotes Neuronal Apoptosis in a 6-OHDA-Toxicant Model of Parkinson's Disease by Inhibiting the Sonic Hedgehog Signaling Pathway.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2024
    Article
  13. Article
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  20. A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain.Medical science monitor : international medical journal of experimental and clinical research · 2022
    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

18 authors at 8 institutions in 4 countries.

Christian M SimonInstitute for Clinical Neurobiology, University of Würzburg, Versbacher-Str. 5, 97078, Würzburg, Germany.
Stefanie Rauskolb
Jennifer M Gunnersen
Bettina Holtmann
Carsten Drepper
Benjamin Dombert
Massimiliano Braga
Stefan Wiese
Sibylle Jablonka
Dirk Pühringer
Jürgen Zielasek
Andreas Hoeflich
Vincenzo Silani
Eckhard Wolf
Susanne Kneitz
Claudia Sommer
Klaus V Toyka
Michael Sendtner
University of Würzburg · DEFerrari (Italy) · ITHeinrich Heine University Düsseldorf · DELudwig-Maximilians-Universität München · DEResearch Institute for Farm Animal Biology (FBN) · DERuhr University Bochum · DEThe University of Melbourne · AUUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic neuropathy (DNP), afflicting sensory and motor nerve fibers, is a major complication in diabetes. The underlying cellular mechanisms of axon degeneration are poorly understood. IGFBP5, an inhibitory binding protein for insulin-like growth factor 1 (IGF1) is highly up-regulated in nerve biopsies of patients with DNP. We investigated the pathogenic relevance of this finding in transgenic mice overexpressing IGFBP5 in motor axons and sensory nerve fibers. These mice develop motor axonopathy and sensory deficits similar to those seen in DNP. Motor axon degeneration was also observed in mice in which the IGF1 receptor (IGF1R) was conditionally depleted in motoneurons, indicating that reduced activity of IGF1 on IGF1R in motoneurons is responsible for the observed effect. These data provide evidence that elevated expression of IGFBP5 in diabetic nerves reduces the availability of IGF1 for IGF1R on motor axons, thus leading to progressive neurodegeneration. Inhibition of IGFBP5 could thus offer novel treatment strategies for DNP.

Indexed as

AnimalsAxonsCarrier ProteinsCell EnlargementCells, CulturedCell SurvivalDiabetes Mellitus, ExperimentalDiabetic NeuropathiesHumansMice, TransgenicMotor ActivityMotor NeuronsNerve DegenerationPhrenic NerveReceptor, IGF Type 1Sciatic NerveCarrier ProteinsIGFBP5-interacting protein, mouseReceptor, IGF Type 1

Identifiers

PMID26025657
PMCPMC4541707
OpenAlexW1569155484

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.