Evidence map›Paper›PMID 41653250›Full record

ArticleMolecular biology reports2026

Endometriosis-derived exosomal MicroRNA-125b-5p downregulates phosphatidylinositol 3-Kinase/Protein Kinase B signaling pathways via vascular endothelial growth factor to decelerate endometriosis progression.

Lei Zhang, Litong Zhu, Huangjin Luo, Xiaolin Chen, Guiyuan Yu, Qiuxia Li, Mo Chen, Ping Jin, Qiuling Shi

Abstract read
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Lei ZhangState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, China.
Litong ZhuDepartment of Gynecology, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong, China.
Huangjin LuoDepartment of Gynecology, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian, People's Republic of China.
Xiaolin ChenDepartment of Gynecology, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong, China.
Guiyuan YuDepartment of Gynecology, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong, China.
Qiuxia LiDepartment of Gynecology, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong, China.
Mo ChenDepartment of Gynecology, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong, China.
Ping JinState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, China. 13925206896@163.com.
Qiuling ShiState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, China. qshi@cqmu.edu.cn.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515220099Sanming Project of Medicine in Shenzen Municipality SZSM202211020Science, Technology and Innovation Commission of Shenzhen Municipality JCYJ20210324130400002Shanghai Pujiang Programme 23PJD009
6 · The paper itself

Abstract

backgroundEndometriosis (EMs) is a chronic enigmatic gynecological disorder which pathogenesis have not been fully elucidated. Exosomes have been proven to participate in endometriosis. However, the role of exosomes in the pathogenesis of EMs remains poorly defined.

methodsExosomes were isolated from cyst fluid of EMs patients and pelvic fluid of non-EMs patients, and characterized by transmission electron microscopy, nanoparticle tracking analysis and western blot. Exosomal miRNAs were performed by small RNA sequencing. Q-PCR and cell function were performed to identify the relationship between exosomal miRNAs and endometriosis. Dual luciferase reporter assay, cell transfection, Q-PCR, Western blotting and CCK8 assays, Transwell assays and Boyden assays were conducted to explore the regulatory effects of exosomal miRNA on EMs pathogenesis in vitro using primary human endometrial stromal cells (HESCs) derived from endometriotic lesions.

resultsCompare with non-EMs group, there are 118 miRNAs were up-regulated and 40 miRNAs were down-regulated in CF group, meanwhile 22 miRNAs were up-regulated and 32 miRNAs were down-regulated in PF group. Q-PCR verified that miR-125b-5p, miR-328-3p, miR-125a-5p, miR-30e-3p were significant down-regulated, whereas miR-3141, miR-223-3p, miR-142-5p, miR-1246 were significant up-regulated in EMs patients. ROC analysis indicated that miR-125b-5p (AUC = 0.925, p < 0.001) was highly correlated with EMs pathogenesis. Dual luciferase reporter assay results demonstrated miR-125b-5p directly targeted VEGF gene. MiR-125b-5p suppressed endometrial stromal cells proliferation, migration and invasion by regulating the Phosphatidylinositol 3-Kinase (PI3K) /Protein Kinase B (AKT) signaling pathway.

conclusionExosomal miR-125b-5p was highly correlated with EMs, and it regulates the PI3K/Akt signaling pathways through VEGF to inhibit endometrial stromal cells proliferation, migration and invasion, acting as an important suppressing miRNA in endometriosis pathogenesis.

Indexed as

EndometriosisExosomesMicroRNAsProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AAdultCell MovementCell ProliferationDisease ProgressionDown-RegulationEndometriumFemaleHumansPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesSignal TransductionMicroRNAsMIRN125 microRNA, humanPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AVEGFA protein, humanEndometriosis pathogenesisExosomeMiRNAPI3K/Akt signaling pathwaysVEGF

Identifiers

PMID41653250
PMCPMC12882959

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.