Evidence map›Paper›PMID 40254638›Full record

ArticleScientific reports2025

Integrated multi-omics analysis and experimental verification reveal the involvement of the PI3K/Akt signaling pathway in myometrial fibrosis of adenomyosis.

Qiaomei Yang, Jingxuan Hong, Jianhui Fu, Xianhua Liu, Xinye Zheng, Junying Jiang, An Zhu, Li Chen, Hao Lin, PengMing Sun

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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Observational
  2. Article
  3. Review
  4. Divergent Associations of the VEGF (Medicina (Kaunas, Lithuania) · 2026
    Article
  5. Article
  6. Review
  7. Signaling pathways and advances in targeted therapy for adenomyosis.Frontiers in cell and developmental biology · 2025
    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.

Qiaomei Yang *College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Jingxuan Hong *Department of Cardiology, Fujian Provincial Hospital Facilitated to Fuzhou University, Fujian Provincial Center for Cardiovascular Epidemiology Research and Prevention, Fuzhou, China.
Jianhui Fu *Department of Pathology, Fujian Maternity and Child Health Hospital College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Xianhua LiuDepartment of Pathology, Fujian Maternity and Child Health Hospital College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Xinye ZhengCollege of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Junying JiangCollege of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
An ZhuKey Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Li ChenCollege of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Hao LinCollege of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
PengMing SunCollege of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China. sunfemy@hotmail.com.

Funding

Fujian Provincial Health Technology Project 2023CXA039Fujian Provincial Natural Science Foundation of China 2023J011216Joint Funds for the Innovation of Science and Technology of Fujian Province 2023Y9391
6 · The paper itself

Abstract

Adenomyosis (AM) is characterized as a chronic and progressive disorder with limited therapeutic strategies available. Myometrial fibrosis is a prominent pathological feature of AM, yet the underlying molecular mechanisms remain elusive. The present study conducted a comparative analysis using proteomics and metabolomics to investigate myometrial fibrosis and its underlying mechanisms. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was utilized to analyze adenomyotic and normal myometrial tissues from ten AM patients who underwent hysterectomy with myometrial fibrosis confirmed by Masson staining. This analysis established comprehensive proteomic and metabolomic profiles of AM patients and revealed widespread alterations in the proteome and metabolome within normal and fibrotic myometrium. Key proteins and signaling pathways linked to myometrial fibrogenesis were identified based on proteomic data. The integrated analysis showed significant associations between proteomic and metabolomic data and highlighted the critical role of the PI3K/AKT signaling pathway. Immunohistochemistry and Spearman's correlation analysis suggested a relationship between myometrial fibrosis and the metaplasia of myometrial stromal cells into myofibroblasts. Subsequent experiments identified crucial proteins and signaling pathways involved in myometrial fibrosis, indicating an association with the activation of the PI3K/AKT signaling pathway in myofibroblasts. Notably, PI3K/AKT inhibitors may contribute to the effective alleviation of myometrial fibrosis. This study is the first to demonstrate that myometrial fibrosis represents a critical pathological mechanism in AM through multi-omics methods and to elucidate the crucial role of the PI3K/AKT signaling pathway in this process. These findings provide valuable insights into the pathophysiology of AM and suggest antifibrotic treatment as a promising therapeutic strategy.

Indexed as

AdenomyosisMyometriumPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAdultChromatography, LiquidFemaleFibrosisHumansMetabolomicsMiddle AgedMultiomicsProteomeProteomicsTandem Mass SpectrometryPhosphatidylinositol 3-KinasesProteomeProto-Oncogene Proteins c-aktAdenomyosisExperimental verificationExtracellular matrix proteinsFibrosisMulti-omicsPI3K/Akt signaling pathway

Identifiers

PMID40254638
PMCPMC12010003

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.