Evidence map›Paper›PMID 41295860›Full record

ArticleToxins2025

The Activities of Recombinant Botulinum Toxin A on Spared Nerve Injury-Induced Neuropathic Pain in a Diabetic Mice Model.

Akinyemi Ademola Omoniyi, Rasmus Eich Hammer, Sabrina Josefsen, Mette Richner, Stephane Lezmi, Christian Bjerggaard Vægter, Mikhail Kalinichev, Páll Karlsson, Jens Randel Nyengaard

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxins, 2025. 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

9 authors.

Akinyemi Ademola OmoniyiCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, 8200 Aarhus N, Denmark.
Rasmus Eich HammerCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, 8200 Aarhus N, Denmark.ORCID 0009-0002-7582-3522
Sabrina JosefsenCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, 8200 Aarhus N, Denmark.ORCID 0009-0005-1687-5885
Mette RichnerDanish Research Institute of Translational Neuroscience (DANDRITE), Nordic-EMBL Partnership for Molecular Medicine, Department of Biomedicine, Aarhus University, 8000 Aarhus C, Denmark.
Stephane LezmiIpsen Innovation, Avenue du Canada, 91940 Les Ulis, France.
Christian Bjerggaard VægterDanish Research Institute of Translational Neuroscience (DANDRITE), Nordic-EMBL Partnership for Molecular Medicine, Department of Biomedicine, Aarhus University, 8000 Aarhus C, Denmark.ORCID 0000-0001-6573-146X
Mikhail KalinichevIpsen Innovation, Avenue du Canada, 91940 Les Ulis, France.ORCID 0000-0001-6621-6339
Páll KarlssonCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, 8200 Aarhus N, Denmark.
Jens Randel NyengaardCore Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Aarhus University, 8200 Aarhus N, Denmark.ORCID 0000-0002-8084-4646

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic neuropathy is characterized by nerve damage and chronic neuropathic pain and lacks effective treatment. Botulinum neurotoxin type A (BoNT/A), a neurotoxin with established therapeutic use in neurological disorders, has emerged as a potential analgesic agent. This study investigated the effects of a recombinant form of BoNT/A1 (rBoNT/A1) on neuropathic pain induced by spared nerve injury (SNI) in a diabetic mouse model. Thirty-two adult male C57BL/6JRj diabetic mice were subjected to SNI or sham surgery. Fourteen days post surgery, mice received an intraplantar dose of rBoNT/A1 or vehicle. Mechanical allodynia was assessed using von Frey filaments, and spinal cord and sciatic nerve tissues were analyzed via immunohistochemistry and transmission electron microscopy to evaluate glial activation, neurotransmitter receptor expression, and axonal morphology. The results demonstrated that rBoNT/A1 significantly alleviated mechanical allodynia and caused a marked reduction in Iba1-positive microglial activation in the spinal cord, whereas no significant changes were observed in astrocyte (GFAP) density or GABAAR subunit expression. Additionally, rBoNT/A1 treatment did not significantly alter axon diameter, myelin thickness, or C-fiber morphology. In conclusion, intraplantar administration of rBoNT/A1 reduced SNI-induced mechanical allodynia in diabetic mice, potentially by attenuating spinal microglial activation, supporting the therapeutic promise of rBoNT/A1 in managing diabetic neuropathic pain.

Indexed as

AnalgesicsBotulinum Toxins, Type ADiabetes Mellitus, ExperimentalDiabetic NeuropathiesNeuralgiaAnimalsDisease Models, AnimalHyperalgesiaMaleMiceMice, Inbred C57BLMicrogliaRecombinant ProteinsSciatic NerveSpinal CordAnalgesicsBotulinum Toxins, Type ARecombinant Proteinsastrocytesdiabetic neuropathyGFAPIba1microgliaperipheral nervous systemvon Frey

Identifiers

PMID41295860
PMCPMC12656591

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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.