Evidence map›Paper›PMID 32392916›Full record

ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2020

Oxysterol 25-hydroxycholesterol as a metabolic pathophysiological factors of osteoarthritis induces apoptosis in primary rat chondrocytes.

Yo-Seob Seo, In-A Cho, Tae-Hyeon Kim, Jae-Seek You, Ji-Su Oh, Gyeong-Je Lee, Do Kyung Kim, Jae-Sung Kim

Open access · diamondAbstract read
In one paragraph

Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Interleukin-1β-induced arthritis involves chondrocyte oxiapoptophagy.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  3. Article
  4. Dexamethasone regulates gene expression in chondrocytes through MKP-1 and downregulates cholesterol hydroxylases CH25H and CYP7B1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  5. Review
  6. 25-Hydroxycholesterol in health and diseases.Journal of lipid research · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

8 authors at 1 institution in 1 country.

Yo-Seob SeoDepartment of Oral and Maxillofacial Radiology, Chosun University, Gwangju 61452, Korea.
In-A ChoInstitute of Dental Science, Chosun University, Gwangju 61452, Korea.
Tae-Hyeon KimInstitute of Dental Science, Chosun University, Gwangju 61452, Korea.
Jae-Seek YouDepartments of Oral and Maxillofacial Surgery, School of Dentistry, Chosun University, Gwangju 61452, Korea.
Ji-Su OhDepartments of Oral and Maxillofacial Surgery, School of Dentistry, Chosun University, Gwangju 61452, Korea.
Gyeong-Je LeeDepartments of Prosthodontics, School of Dentistry, Chosun University, Gwangju 61452, Korea.
Do Kyung KimInstitute of Dental Science, Chosun University, Gwangju 61452, Korea.
Jae-Sung KimInstitute of Dental Science, Chosun University, Gwangju 61452, Korea.
Chosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the pathophysiological etiology of osteoarthritis that is mediated by the apoptosis of chondrocytes exposed to 25-hydroxycholesterol (25-HC), an oxysterol synthesized by the expression of cholesterol-25-hydroxylase (CH25H) under inflammatory conditions. Interleukin-1β induced the apoptosis of chondrocytes in a dose- dependent manner. Furthermore, the production of 25-HC increased in the chondrocytes treated with interleukin-1β through the expression of CH25H. 25-HC decreased the viability of chondrocytes. Chondrocytes with condensed nucleus and apoptotic populations increased by 25-HC. Moreover, the activity and expression of caspase-3 were increased by the death ligand-mediated extrinsic and mitochondria-dependent intrinsic apoptotic pathways in the chondrocytes treated with 25-HC. Finally, 25-HC induced not only caspase-dependent apoptosis, but also induced proteoglycan loss in articular cartilage

Indexed as

25-HydroxycholesterolApoptosisCholesterolChondrocytesOsteoarthritis

Identifiers

PMID32392916
PMCPMC7193916
OpenAlexW3023252845

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.