ArticleFrontiers in pharmacology2025
Role of biomarker SOCS1 in peritoneal dialysis-associated peritoneal fibrosis and immune infiltration based on machine learning screening.
Article in Frontiers in pharmacology, 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.
- Peritoneal dialysis effluent biomarkers from a multi-omics and artificial intelligence perspective: advances and challenges.Clinical kidney journal · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction/Objectives: Chronic peritoneal dialysis (PD) induces peritoneal fibrosis through bioincompatible fluid exposure and inflammation. This study aimed to identify fibrosis biomarkers via bioinformatics, assess immune cell correlations, and validate diagnostic utility in clinical/animal models. Methods: We analyzed the GSE125498 peritoneal fluid transcriptome to identify differentially expressed genes (DEGs). Functional enrichment, protein interaction networks, and pathway analyses were performed. Three machine learning algorithms screened diagnostic markers, validated by ROC curves and nomogram modeling. Immune infiltration patterns were correlated with biomarkers. Clinical validation included SOCS-1/TGF-β1 quantification in 86 PD patients' effluent and a CKD rat fibrosis model to assess SOCS-1/TGF-β/Smad pathway interactions. Results: Four hub genes (PIM2, HSH2D, MYO3B, SOCS1; AUC = 0.914) were identified as PD fibrosis biomarkers. Monocyte infiltration increased significantly in long-term PD cohorts and inversely correlated with all biomarkers. SOCS1 exhibited positive associations with CD4+/CD8+ T cells and M1 macrophages, but negative correlations with resting mast cells and monocytes. Clinically, SOCS-1 levels in PD effluent showed non-linear temporal dynamics. Rat models confirmed SOCS-1 overexpression in fibrotic peritoneum and its functional link to TGF-β/Smad signaling. Conclusion: SOCS-1 emerges as a novel biomarker for PD-related peritoneal fibrosis, with monocyte-mediated mechanisms playing a critical role. Animal studies implicate SOCS-1 in TGF-β/Smad-driven fibrogenesis. These findings provide mechanistic insights and translational tools for monitoring PD complications.
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.