ArticleEuropean journal of medical research2025
Cross-talk between mitophagy pathways in pre-eclampsia and gestational diabetes mellitus: a systematic analysis of shared molecular mechanisms.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Enhancing Early Prediction of Gestational Diabetes Mellitus Through Data Augmentation and Feature Guidance: Model Development and Validation Study.JMIR medical informatics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundMitophagy plays a crucial role in both pre-eclampsia (PE) and gestational diabetes mellitus (GDM); however, the molecular mechanisms connecting these conditions remain unclear. This study employs bioinformatics approaches to investigate shared mitophagy-related gene signatures in PE and GDM.
methodsWe analyzed RNA sequencing data from PE and GDM patients to identify mitophagy-related differentially expressed genes (MRDEGs). Diagnostic models were constructed using RandomForest, LASSO and Nomogram, with validation through decision curve analysis (DCA) and calibration curves. Functional enrichment and regulatory networks involving MRDEGs, miRNAs and transcription factors (TFs) were constructed. Expression of key genes was subsequently validated in placental tissues through quantitative analysis.
resultsA total of 11 MRDEGs were identified. The LASSO model demonstrated promising diagnostic potential, achieving AUC values of 0.646 for PE and 0.721 for GDM. Eight key MRDEGs were closely associated with oxidative phosphorylation and reactive oxygen species (ROS) signaling pathways. Immune infiltration analysis revealed significant alterations in immune cell infiltration levels in both PE and GDM placental tissues, particularly manifesting as notable decreases in activated CD4 T cells and activated dendritic cells. These MRDEGs interacted with 80 TFs and 101 miRNAs in comprehensive regulatory networks. Finally, validation in placental tissues from control (n = 24) and disease groups (PE: n = 18, GDM: n = 20) confirmed significant differential expression of five key genes (MRPS5, PNPO, ARRB2, UBE2M, and PRAGC; all P < 0.01).
conclusionsThis study highlights key MRDEGs as potential diagnostic biomarkers for PE and GDM, with their differential expression substantiated in placental tissues. Mitophagy likely contributes to disease pathogenesis through immune regulation and oxidative stress mechanisms, offering novel perspectives on potential therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.