Evidence map›Paper›PMID 39882333›Full record

ArticleBiomedical reports2025

Age‑related changes in endoplasmic reticulum stress response‑associated protein expression in rat tibial nerves.

Masahiro Sakita, Wataru Isobe, Koji Nonaka, Shinichiro Murakami, Ryo Miyachi, Kento Sakane, Saki Sugimoto, Airi Yamaguchi, Koki Yamamoto

Abstract read
In one paragraph

Article in Biomedical 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

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

1 citing paper in PubMed.

  1. 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

9 authors.

Masahiro SakitaDepartment of Physical Therapy, Faculty of Health Sciences, Kyoto Tachibana University, Kyoto 607-8175, Japan.
Wataru IsobeDepartment of Physical Therapy, Faculty of Health Sciences, Kyoto Tachibana University, Kyoto 607-8175, Japan.
Koji NonakaDepartment of Rehabilitation, Faculty of Health Care Sciences, Naragakuen University, Nara 631-0003, Japan.
Shinichiro MurakamiDepartment of Physical Therapy, Faculty of Health Care Sciences, Himeji-Dokkyo University, Himeji, Hyogo 670-0896, Japan.
Ryo MiyachiDepartment of Physical Therapy, Faculty of Health Care Sciences, Hokuriku University, Kanazawa, Ishikawa 920-1154, Japan.
Kento SakaneDepartment of Physical Therapy, Faculty of Health Sciences, Kyoto Tachibana University, Kyoto 607-8175, Japan.
Saki SugimotoDepartment of Physical Therapy, Faculty of Health Sciences, Kyoto Tachibana University, Kyoto 607-8175, Japan.
Airi YamaguchiDepartment of Physical Therapy, Faculty of Health Sciences, Kyoto Tachibana University, Kyoto 607-8175, Japan.
Koki YamamotoDepartment of Physical Therapy, Faculty of Health Sciences, Kyoto Tachibana University, Kyoto 607-8175, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In age-related peripheral neurodegeneration, changes in the promotion or inhibition of endoplasmic reticulum (ER) stress response related to the ubiquitin-proteasome degradation system (UPS), autophagy and apoptosis signaling factors during aging remain unclear. In the present study, the expression of ER stress response signaling-related protein factors was examined in tibial nerves during aging in rats. Tibial nerves were extracted from continuously housed rats at 20, 50, 70, 90 and 105 weeks of age. Expression of factors associated with ER stress-related degradation, including X-box binding protein 1 (XBP1s), eukaryotic translation initiation factor 2 subunit 1 (eIF2α), Beclin-1 (Becn1), and Caspase-3 (Casp3); ER stress-related repair, including binding immunoglobulin protein [also known as 78 kDa glucose-regulated protein (BiP/GRP78)], protein disulfide isomerase (PDI), brain-derived neurotrophic factor (BDNF) and the inflammatory cytokine IL6, was assessed by western blotting of tibial nerves from rats in each age group. Expression of XBP1s and Becn1, which promote UPS and autophagy, decreased significantly after 50 weeks of age. However, expression of eIF2α and Casp3, which inhibit new protein biosynthesis and promote apoptosis, increased significantly after 50 weeks. Expression of BiP/GRP78 and PDI, which are refolding factors for denatured proteins, showed a significant decrease after 50 (or 70) weeks of age. The expression of BDNF, a ligand protein for the repair cascade, showed a significant increase after 70 weeks of age, while that of IL6 increased significantly after 50 weeks of age. These results indicate that ER stress-related degradation (UPS and autophagy) and refolding repair functions are reduced in rat tibial nerves after 50 weeks, followed by enhanced apoptosis and inflammation. These findings shed light on the progression of age-related peripheral neurodegeneration in rats.

Indexed as

agingapoptosisautophagyendoplasmic reticulumneurodegenerationtibial nerveubiquitin-proteasome degradation system

Identifiers

PMID39882333
PMCPMC11775640

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.