Evidence map›Paper›PMID 40461537›Full record

ArticleScientific reports2025

The effects of inhibiting IRE1α on the viability of ovarian granulosa cells.

Chao Li, Yong-Peng Tan, Tie-Gang Meng, Di Gao, Ke Xu, You-Hui Lu, Li-Tao Yi, Shu-Chen Liu, Guang Wang, Qing-Yuan Sun and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Chao Li *Guangdong Second Provincial General Hospital, Postdoctoral Research Station of Basic Medicine, School of Medicine, Jinan University, Guangzhou, 510317, China.
Yong-Peng Tan *Guangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Tie-Gang Meng *Guangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Di GaoGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Ke XuGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
You-Hui LuGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Li-Tao YiGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Shu-Chen LiuGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Guang WangGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China. wangguang7453@126.com.
Qing-Yuan SunGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China. sunqy@gd2h.org.cn.
Xiao-Can LeiClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, China. 2019000013@usc.edu.cn.

Funding

Science and Technology Program of Guangzhou, China 2023A03J0258
6 · The paper itself

Abstract

IRE1α, a type I transmembrane protein characterized by a cytoplasmic serine/threonine kinase domain, is related to ER stress and ER function maintenance. In this study, 4µ8c, a highly effective selective inhibitor of IRE1α RNase, and APY29, an ATP competitive inhibitor, inhibiting IRE1α autophosphorylation and the kinase domain, were employed to elucidate the function of IRE1α on the proliferation of ovarian granulosa cells, with the ultimate goal of identifying novel strategies and methodologies for the prevention and treatment of associated diseases. Human ovarian granulosa cells (SVOG) cultured in vitro were treated with the IRE1α inhibitors 4µ8c and APY29. It was shown that inhibition of IRE1α reduced the cell ability of dealing with misfolded protein, triggered oxidative stress, altered mitochondrial membrane potential, and inflicted DNA damage, eventually lead to ovarian granulosa cell apoptosis.

Indexed as

EndoribonucleasesGranulosa CellsProtein Serine-Threonine KinasesApoptosisCell ProliferationCells, CulturedCell SurvivalDNA DamageEndoplasmic Reticulum StressFemaleHumansMembrane Potential, MitochondrialOxidative StressPhosphorylationEndoribonucleasesERN1 protein, humanProtein Serine-Threonine Kinases4µ8cAPY29Cell apoptosisChaperonesIRE1αOvarian granulosa cells

Identifiers

PMID40461537
PMCPMC12134056

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.