Evidence map›Paper›PMID 31150519›Full record

ArticlePloS one2019

Chemical proteasome inhibition as a novel animal model of inner retinal degeneration in rats.

Masaaki Kageyama, Takashi Ota, Masaaki Sasaoka, Osamu Katsuta, Katsuhiko Shinomiya

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The Role of the Ubiquitin System in Eye Diseases.Life (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Proteostasis in aging-associated ocular disease.Molecular aspects of medicine · 2022
    Review
  9. Article
  10. 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

5 authors at 1 institution in 1 country.

Masaaki KageyamaGlobal Alliances and External Research, Santen Pharmaceutical Co., Ltd., Nara, Japan.ORCID 0000-0002-6520-7905
Takashi OtaGlobal Alliances and External Research, Santen Pharmaceutical Co., Ltd., Nara, Japan.
Masaaki SasaokaGlobal Alliances and External Research, Santen Pharmaceutical Co., Ltd., Nara, Japan.
Osamu KatsutaResearch and Development Center, Santen Pharmaceutical Co., Ltd., Nara, Japan.
Katsuhiko ShinomiyaResearch and Development Center, Santen Pharmaceutical Co., Ltd., Nara, Japan.
Santen (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemical proteasome inhibition has been a valuable animal model of neurodegeneration to uncover roles for the ubiquitin-proteasome system in the central nervous system. However, little is known about the effects of chemical proteasome inhibitors on retinal integrity. Therefore, we characterized the effects of structurally different chemical proteasome inhibitors on the retinal morphology and the mechanisms of their action in the normal adult rat eyes. Intravitreal injection of MG-262 and other proteasome inhibitors led to inner retinal degeneration. MG-262-induced inner retinal degeneration was accompanied by reduced proteasome activity, increased poly-ubiquitinated protein levels, and increased positive immunostaining of ubiquitin, 20S proteasome subunit and GADD153/CHOP in the retina. Its retinal degenerative effect was also associated with reduced retinal neurofilament light chain gene expression, reflecting retinal ganglion cell death. MG-262-induced neurofilament light chain downregulation was largely resistant to pharmacological modulation including endoplasmic reticulum stress, apoptosis or MAP kinase inhibitors. Thus, this study provides further evidence of roles for the ubiquitin-proteasome system in the maintenance of the retinal structural integrity. Chemical proteasome inhibition may be used as a novel animal model of inner retinal degeneration, including retinal ganglion cell loss, which warrants further analysis of the molecular mechanisms underlying its retinal degenerative effect.

Indexed as

AnimalsApoptosisBoronic AcidsDisease Models, AnimalEndoplasmic ReticulumEndoplasmic Reticulum StressHumansProteasome Endopeptidase ComplexProteasome InhibitorsRatsRetinaRetinal DegenerationRetinal Ganglion CellsThapsigarginTunicamycinBoronic AcidsMG 262Proteasome Endopeptidase ComplexProteasome InhibitorsThapsigarginTunicamycin

Identifiers

PMID31150519
PMCPMC6544319
OpenAlexW2947681828

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.