Evidence map›Paper›PMID 31882756›Full record

ArticleScientific reports2019

Histone acetyltransferase and Polo-like kinase 3 inhibitors prevent rat galactose-induced cataract.

Fumito Kanada, Yoshihiro Takamura, Seiji Miyake, Kazuma Kamata, Mayumi Inami, Masaru Inatani, Masaya Oki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Current Approach to the Pathogenesis of Diabetic Cataracts.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Fumito KanadaDepartment of Applied Chemistry and Biotechnology, Graduate School of Engineering, University of Fukui, Fukui, 910-8507, Japan.
Yoshihiro TakamuraDepartment of Ophthalmology, Faculty of Medical Sciences, University of Fukui, Fukui, 910-1193, Japan.
Seiji MiyakeDepartment of Ophthalmology, Faculty of Medical Sciences, University of Fukui, Fukui, 910-1193, Japan.
Kazuma KamataDepartment of Applied Chemistry and Biotechnology, Graduate School of Engineering, University of Fukui, Fukui, 910-8507, Japan.
Mayumi InamiDepartment of Applied Chemistry and Biotechnology, Graduate School of Engineering, University of Fukui, Fukui, 910-8507, Japan.
Masaru InataniDepartment of Ophthalmology, Faculty of Medical Sciences, University of Fukui, Fukui, 910-1193, Japan.
Masaya OkiDepartment of Applied Chemistry and Biotechnology, Graduate School of Engineering, University of Fukui, Fukui, 910-8507, Japan. ma4sa6ya@u-fukui.ac.jp.
University of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cataracts can occur at an early age, causing visual impairment or blindness. The detailed molecular mechanisms of diabetic cataract formation remain incompletely understood, and there is no well-documented prophylactic agent. Galactose-fed rats and ex vivo treatment of lenses with galactose are used as models of diabetic cataract. To assess the role of histone acetyltransferases, we conducted cataract prevention screening with known histone acetyltransferase (HAT) inhibitors. Ex vivo treatment with a HAT inhibitor strongly inhibited the formation of lens turbidity in high-galactose conditions, while addition of a histone deacetylase (HDAC) inhibitor aggravated turbidity. We conducted a microarray to identify genes differentially regulated by HATs and HDACs, leading to discovery of a novel cataract causative factor, Plk3. Plk3 mRNA levels correlated with the degree of turbidity, and Plk3 inhibition alleviated galactose-induced cataract formation. These findings indicate that epigenetically controlled Plk3 influences cataract formation. Our results demonstrate a novel approach for prevention of diabetic cataract using HAT and Plk3 inhibitors.

Indexed as

AnimalsCataractCell Cycle ProteinsDiabetes Mellitus, ExperimentalEnzyme InhibitorsGalactoseHistone AcetyltransferasesLens, CrystallineProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyCell Cycle ProteinsEnzyme InhibitorsGalactoseHistone AcetyltransferasesPlk3 protein, ratProtein Serine-Threonine Kinases

Identifiers

PMID31882756
PMCPMC6934598
OpenAlexW2998281421

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.