Evidence map›Paper›PMID 40865634›Full record

ArticleJournal of advanced research2026

Exploration and analysis of methylglyoxal-driven chronic inflammation in polycystic ovary syndrome.

Jiahui Song, Xiao Wang, Di Feng, Wenyan Gao, Xinmei Wang, Xinzhu Qiu, Wanting Cheng, Yuanyuan Fang, Bei Shi, Da Li

Abstract read
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

10 authors.

Jiahui SongCenter of Reproductive Medicine, Shengjing Hospital of China Medical University, Shenyang, China; NHC Key Laboratory of Advanced Reproductive Medicine and Fertility (China Medical University), National Health Commission, Shenyang, China; School of Forensic Medicine, China Medical University, Shenyang, China.
Xiao WangDepartment of Physiology, School of Life Sciences, China Medical University, Shenyang, China; Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China; Department of Epidemiology, School of Public Health, China Medical University, Shenyang, China.
Di FengCenter of Reproductive Medicine, Shengjing Hospital of China Medical University, Shenyang, China; NHC Key Laboratory of Advanced Reproductive Medicine and Fertility (China Medical University), National Health Commission, Shenyang, China; Education Center for Clinical Skills Practice, China Medical University, Shenyang, China.
Wenyan GaoDepartment of Obstetrics, the First Affiliated Hospital of China Medical University, Shenyang, China; Key Laboratory of Reproductive Dysfunction Diseases and Fertility Remodeling of Liaoning Province, Shenyang, China.
Xinmei WangDepartment of Physiology, School of Life Sciences, China Medical University, Shenyang, China.
Xinzhu QiuDepartment of Physiology, School of Life Sciences, China Medical University, Shenyang, China.
Wanting ChengDepartment of Physiology, School of Life Sciences, China Medical University, Shenyang, China.
Yuanyuan FangCenter of Reproductive Medicine, Shengjing Hospital of China Medical University, Shenyang, China; NHC Key Laboratory of Advanced Reproductive Medicine and Fertility (China Medical University), National Health Commission, Shenyang, China; Key Laboratory of Reproductive Dysfunction Diseases and Fertility Remodeling of Liaoning Province, Shenyang, China. Electronic address: fangyy_sj@sina.com.
Bei ShiCenter of Reproductive Medicine, Shengjing Hospital of China Medical University, Shenyang, China; NHC Key Laboratory of Advanced Reproductive Medicine and Fertility (China Medical University), National Health Commission, Shenyang, China; Department of Physiology, School of Life Sciences, China Medical University, Shenyang, China. Electronic address: bshi@cmu.edu.cn.
Da LiCenter of Reproductive Medicine, Shengjing Hospital of China Medical University, Shenyang, China; NHC Key Laboratory of Advanced Reproductive Medicine and Fertility (China Medical University), National Health Commission, Shenyang, China; Key Laboratory of Reproductive Dysfunction Diseases and Fertility Remodeling of Liaoning Province, Shenyang, China. Electronic address: leeda@ymail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic low-grade inflammation drives polycystic ovary syndrome (PCOS)-related metabolic disorders, but the underlying mechanisms remain unclear. Methylglyoxal, a key ovarian metabolite, promotes inflammation when elevated, its role in PCOS-related inflammation remains uncharacterized.

objectivesThis study aimed to identify the role of methylglyoxal in PCOS-related inflammation and its mechanisms of action.

methodsThis study recruited 258 participants from Shengjing Hospital. White blood cells, neutrophils, and lymphocytes were counted. The Olink Target 96 Inflammation Panel and untargeted metabolomics were used to determine the expression levels of inflammatory factors and metabolites. Key metabolites regulating inflammation were investigated via multiomics analysis (transcriptomics, proteomics, and metabolomics) and machine learning. The levels of methylglyoxal and inflammatory molecules were measured via ELISA. Restricted cubic spline, linear/logistic regression, and receiver operating characteristic (ROC) analyses were performed to examine the relationship between methylglyoxal levels and inflammation.

resultsMethylglyoxal levels were notably higher in the follicular fluid and serum of PCOS patients, closely linked to inflammation. Even after adjusting for confounding factors, elevated methylglyoxal levels remained an independent risk factor for inflammatory markers in PCOS patients. In PCOS, insulin resistance and dyslipidemia are associated with increased methylglyoxal concentrations and a more pronounced relationship between methylglyoxal and inflammatory processes. Compared with individuals with normal weight and low methylglyoxal levels, those who were obese or overweight and had high levels of methylglyoxal showed severe inflammatory responses. Additionally, multiomics analysis indicated that IL-17A may serve as a key downstream factor of methylglyoxal.

conclusionWe observed significantly elevated methylglyoxal levels in both the follicular fluid and serum of PCOS patients, which were strongly associated with inflammation. Serum methylglyoxal shows promise as a novel biomarker for PCOS-related metabolic-inflammatory dysregulation and may provide a novel target for the treatment of PCOS.

Indexed as

InflammationPolycystic Ovary SyndromePyruvaldehydeAdultBiomarkersChronic DiseaseFemaleFollicular FluidHumansInsulin ResistanceMetabolomicsYoung AdultBiomarkersPyruvaldehydeInflammationMethylglyoxalOlink Target 96 Inflammation PanelPolycystic ovary syndromeUntargeted metabolomics

Identifiers

PMID40865634
PMCPMC13131410

What OpenQuestion 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 OpenQuestion graph.