Evidence map›Paper›PMID 42484717›Full record

ArticleMolecular biology reports2026

MiR-126-3p promotes the development and progression of preeclampsia through the inactivation of the PI3K/AKT pathway.

Pingping Zhu, Yanjun Hu, Jiaying Shen, Jianqiong Zheng, Tingting Liao, Yeping Wang

Abstract read
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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. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Pingping ZhuDepartment of Obstetrics, The Wenzhou Third Clinical Institute Affiliated To Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospitalï the city of Wenzhou, Zhejiang, 325000, China.
Yanjun HuDepartment of Obstetrics, The Wenzhou Third Clinical Institute Affiliated To Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospitalï the city of Wenzhou, Zhejiang, 325000, China.
Jiaying ShenDepartment of Obstetrics, Postgraduate training base Allianceof Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospitalï the city of Wenzhou, Zhejiang, China.
Jianqiong ZhengDepartment of Obstetrics, The Wenzhou Third Clinical Institute Affiliated To Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospitalï the city of Wenzhou, Zhejiang, 325000, China.
Tingting LiaoDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying, Children's Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. 15867735780@163.com.
Yeping WangDepartment of Obstetrics, The Wenzhou Third Clinical Institute Affiliated To Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospitalï the city of Wenzhou, Zhejiang, 325000, China. yayawyp@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia (PE) is a severe pregnancy complication that endangers maternal and fetal health. Accumulating evidence indicates that miR-126-3p is aberrantly expressed in PE placentas, yet its specific regulatory mechanism remains poorly defined. In the present study, we confirmed that miR-126-3p was significantly upregulated in placental tissues from PE patients. Functional assays demonstrated that overexpression of miR-126-3p suppressed proliferation, migration and invasion of HTR-8/SVneo trophoblast cells, and induced cell apoptosis, while miR-126-3p knockdown exerted opposite effects. Dual-luciferase reporter assay verified that miR-126-3p directly targeted PIK3R. Further mechanism experiments revealed that miR-126-3p inactivated the PI3K/AKT signaling pathway. Intervention with PI3K agonist and inhibitor further validated that miR-126-3p modulated trophoblast biological behaviors dependent on the PI3K/AKT pathway. In conclusion, elevated miR-126-3p contributes to the development and progression of PE via inhibiting the PI3K/AKT pathway through targeting PIK3R2. This work provides a novel molecular mechanism and potential therapeutic target for PE.

Indexed as

MicroRNAsPhosphatidylinositol 3-KinasesPre-EclampsiaProto-Oncogene Proteins c-aktAdultApoptosisCell LineCell MovementCell ProliferationDisease ProgressionFemaleHumansPlacentaPregnancySignal TransductionTrophoblastsMicroRNAsMIRN126 microRNA, humanPhosphatidylinositol 3-Kinasesphosphoinositol-3 kinase regulatory subunit 2, humanProto-Oncogene Proteins c-aktmiR-126-3p༛PI3K༛proliferation༛invasion ༛migrationPreeclampsia

Identifiers

PMID42484717

What Socratic holds

Textmetadata
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.