ArticleRenal failure2025
Screening potential diagnostic biomarkers for PLA2R‑associated idiopathic membranous nephropathy by WGCNA analysis and LASSO algorithm.
Article in Renal failure, 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.
- The role of serum BAFF, CFB, MCP-1 and anti-PLA2R antibodies in the efficacy evaluation of patients with membranous nephropathy.Journal of medical biochemistry · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adult nephrotic syndrome is primarily caused by membranous nephropathy (MN), with idiopathic membranous nephropathy (IMN) being a prominent subtype. The onset of phospholipase A2 receptor (PLA2R1)-associated IMN is critically linked to M-type PLA2R1 exposure, yet the mechanism underlying glomerular injury remains unclear. In this study, membranous nephropathy datasets (GSE115857, GSE200828) were retrieved from GEO. Differential gene expression was analyzed using the 'limma' R package. WGCNA filtered PLA2R-related modules and intersected genes. LASSO regression, evaluated by ROC analysis, identified characteristic genes. Binomial logistic regression assessed their association with IMN. Validation was performed in the GSE133288 dataset. IHC and qRT-PCR detected characteristic gene expression in PLA2R-positive patients. This study identified elevated PLA2R expression in IMN patients among 117 DEGs. PPI analysis suggested enrichment in Golgi membranes, co-regulation, and glucocorticoid responsiveness, implicating the PPAR pathway by KEGG. WGCNA revealed a 440-gene brown module associated with IMN-PLA2R, with ECM1, SLC19A2, RASD1, FOSB, KDELR3, ZFP36, and ELF4 highlighted as diagnostic markers by ROC analysis. Clinical validation confirmed ECM1 upregulation increased IMN risk, while upregulation of SLC19A2, ZFP36, RASD1, and FOSB decreased it. ECM1 positively correlated with PLA2R, whereas SLC19A2, ZFP36, and FOSB negatively correlated. IHC analysis demonstrated consistent gene expression patterns in IMN tissues, with podocyte exposure to PLA2R-positive serum reducing viability and increasing apoptosis. Functional studies, prompted by RASD1 downregulation, revealed enhanced cell activity and reduced apoptosis upon RASD1 overexpression compared to the Serum + Ov-NC control. Collectively, this study identified diagnostic markers for PLA2R-related IMN, offering novel therapeutic targets for the treatment of IMN.
Indexed as
Identifiers
What Socratic 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 Socratic graph.