Evidence map›Paper›PMID 40052576›Full record

ArticleMolecular medicine reports2025

Glycoprotein 130 improves repressor element‑1 silencing transcription factor‑related axon regenerative capacity in peripheral nerves with aging.

So Kawakita, Kiyohito Naito, Daisuke Kubota, Yuji Ueno, Takako Negishi-Koga, Yasuhiro Yamamoto, Takamaru Suzuki, Norizumi Imazu, Kenjiro Kawamura, Nobutaka Hattori and 1 more

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Article in Molecular medicine reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed.

  1. Review
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

11 authors.

So KawakitaDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.
Kiyohito NaitoDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.
Daisuke KubotaDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.
Yuji UenoDepartment of Neurology, Graduate School of Medical Sciences, University of Yamanashi, Chuo, Yamanashi 409‑3898, Japan.
Takako Negishi-KogaDepartment of Orthopedics, Juntendo University Faculty of Medicine, Tokyo 113‑8421, Japan.
Yasuhiro YamamotoDepartment of Orthopedics, Juntendo University Faculty of Medicine, Tokyo 113‑8421, Japan.
Takamaru SuzukiDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.
Norizumi ImazuDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.
Kenjiro KawamuraDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo 113‑8421, Japan.
Muneaki IshijimaDepartment of Medicine for Orthopedics and Motor Organ, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axon regenerative capacity diminishes with aging and differences in the condition of peripheral nerves between young and elderly individuals have been reported. However, the underlying pathology remains unclear. The expression of repressor element‑1 silencing transcription factor (REST) increases with age and is reported to suppress axon regeneration. The present study investigated the pathology and potential treatment of reduced axon regenerative capacity using REST‑regulated cells and a mouse model. This study examined the molecular expression of the janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) pathway, which is involved in growth‑associated protein 43 (GAP43) expression. In REST‑overexpressed (REST‑OE), glycoprotein 130 (GP130), JAK1 and phosphorylated STAT3 (p‑STAT3) expression was decreased compared with the control (GP130, P=0.004; JAK1, P=0.038; pSTAT3, P=0.015). On the other hand, in REST‑low expressed (siREST), GP130, JAK1 and pSTAT3 expression was increased compared with the control (GP130, P=0.004; JAK1, P=0.003; pSTAT3, P=0.033). It suggested that GP130 plays an important role. Therefore, GP130 agonist was administered to REST‑OE and aged mice and resulted in a significant increase in GAP43 expression (REST‑OE: Protein P=0.018, mRNA P=0.040; aged mice: Protein P=0.016, mRNA P=0.013). The results of this study suggest that the pathology of reduction in peripheral nerve axon regenerative capacity is inhibited by age‑related increase in REST expression, which leads to decreased GP130 expression and inhibition of JAK1/STAT3 pathway activity. These findings suggest that regulating GP130 expression may improve axon regenerative capacity by aging.

Indexed as

AgingAxonsCytokine Receptor gp130Nerve RegenerationPeripheral NervesRepressor ProteinsAnimalsGAP-43 ProteinJanus Kinase 1MaleMiceRE1-Silencing Transcription FactorSignal TransductionSTAT3 Transcription FactorCytokine Receptor gp130GAP-43 ProteinJanus Kinase 1RE1-Silencing Transcription FactorRepressor ProteinsSTAT3 Transcription Factoragingaxon regenerationglycoprotein 130janus kinase 1/signal transducer and activator of transcription 3repressor element 1 silencing transcription factor

Identifiers

PMID40052576
PMCPMC11920774

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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.