Evidence map›Paper›PMID 37355700›Full record

ArticleJournal of neuroinflammation2023

SAFit2 ameliorates paclitaxel-induced neuropathic pain by reducing spinal gliosis and elevating pro-resolving lipid mediators.

Saskia Wedel, Lisa Hahnefeld, Yannick Schreiber, Christian Namendorf, Tim Heymann, Manfred Uhr, Mathias V Schmidt, Natasja de Bruin, Felix Hausch, Dominique Thomas and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  4. Analgesia through FKBP51 inhibition at disease onset confers lasting relief from sensory and emotional chronic pain symptoms.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  5. Neurobiology of stress · 2025
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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

12 authors at 4 institutions in 1 country.

Saskia WedelInstitute of Clinical Pharmacology, Pharmazentrum Frankfurt/ZAFES, University Hospital, Goethe-University, 60590, Frankfurt am Main, Germany.
Lisa HahnefeldInstitute of Clinical Pharmacology, Pharmazentrum Frankfurt/ZAFES, University Hospital, Goethe-University, 60590, Frankfurt am Main, Germany.
Yannick SchreiberFraunhofer Institute for Translational Medicine and Pharmacology ITMP, and Fraunhofer Cluster of Excellence for Immune Mediated Diseases CIMD, 60596, Frankfurt am Main, Germany.
Christian NamendorfCore Unit Analytics and Mass Spectrometry, Max Planck Institute of Psychiatry, 80804, Munich, Germany.
Tim HeymannDepartment of Biochemistry, Technical University of Darmstadt, 64287, Darmstadt, Germany.
Manfred UhrCore Unit Analytics and Mass Spectrometry, Max Planck Institute of Psychiatry, 80804, Munich, Germany.
Mathias V SchmidtCore Unit Analytics and Mass Spectrometry, Max Planck Institute of Psychiatry, 80804, Munich, Germany.
Natasja de BruinFraunhofer Institute for Translational Medicine and Pharmacology ITMP, and Fraunhofer Cluster of Excellence for Immune Mediated Diseases CIMD, 60596, Frankfurt am Main, Germany.
Felix HauschDepartment of Biochemistry, Technical University of Darmstadt, 64287, Darmstadt, Germany.
Dominique ThomasInstitute of Clinical Pharmacology, Pharmazentrum Frankfurt/ZAFES, University Hospital, Goethe-University, 60590, Frankfurt am Main, Germany.
Gerd GeisslingerInstitute of Clinical Pharmacology, Pharmazentrum Frankfurt/ZAFES, University Hospital, Goethe-University, 60590, Frankfurt am Main, Germany.
Marco SisignanoInstitute of Clinical Pharmacology, Pharmazentrum Frankfurt/ZAFES, University Hospital, Goethe-University, 60590, Frankfurt am Main, Germany. Marco.Sisignano@med.uni-frankfurt.de.
Goethe University Frankfurt · DEFraunhofer Institute for Translational Medicine and Pharmacology · DEMax Planck Institute of Psychiatry · DETechnical University of Darmstadt · DE

Funding

Bundesministerium für Bildung und Forschung 51TaValPDeutsche Forschungsgemeinschaft 445757098Deutsche Forschungsgemeinschaft SFB1039 A09Deutsche Forschungsgemeinschaft SFB1039 Z01Fraunhofer-Institut für Translationale Medizin und Pharmakologie Foundation Project Neuropathic PainFraunhofer-Institut für Translationale Medizin und Pharmakologie Fraunhofer Cluster of Excellence for Immune-Mediated Diseases (CIMD)
6 · The paper itself

Abstract

backgroundChemotherapy-induced neuropathic pain (CIPN) describes a pathological pain state that occurs dose-dependently as a side effect and can limit or even impede an effective cancer therapy. Unfortunately, current treatment possibilities for CIPN are remarkably confined and mostly inadequate as CIPN therapeutics themselves consist of low effectiveness and may induce severe side effects, pointing out CIPN as pathological entity with an emerging need for novel treatment targets. Here, we investigated whether the novel and highly specific FKBP51 inhibitor SAFit2 reduces paclitaxel-induced neuropathic pain.

methodsIn this study, we used a well-established multiple low-dose paclitaxel model to investigate analgesic and anti-inflammatory properties of SAFit2. For this purpose, the behavior of the mice was recorded over 14 days and the mouse tissue was then analyzed using biochemical methods.

resultsHere, we show that SAFit2 is capable to reduce paclitaxel-induced mechanical hypersensitivity in mice. In addition, we detected that SAFit2 shifts lipid levels in nervous tissue toward an anti-inflammatory and pro-resolving lipid profile that counteracts peripheral sensitization after paclitaxel treatment. Furthermore, SAFit2 reduced the activation of astrocytes and microglia in the spinal cord as well as the levels of pain-mediating chemokines. Its treatment also increased anti-inflammatory cytokines levels in neuronal tissues, ultimately leading to a resolution of neuroinflammation.

conclusionsIn summary, SAFit2 shows antihyperalgesic properties as it ameliorates paclitaxel-induced neuropathic pain by reducing peripheral sensitization and resolving neuroinflammation. Therefore, we consider SAFit2 as a potential novel drug candidate for the treatment of paclitaxel-induced neuropathic pain.

Indexed as

NeuralgiaPaclitaxelAnimalsGliosisLipidsMiceMorpholinesNeuroinflammatory DiseasesPiperidinesLipidsMorpholinesPaclitaxelPiperidinesSAFit2ChemotherapyFKBP51Neuropathic painOxylipinsSAFit2

Identifiers

PMID37355700
PMCPMC10290418
OpenAlexW4381929645

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.