ArticlePloS one2025
Comprehensive analysis of disulfidptosis-related genes in pulmonary hypertension through machine learning and immune infiltration: Spotlight on USP32 and ZNF655 as key regulators.
Article in PloS one, 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.
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDisulfidptosis, a novel cellular death manner, has yet to be fully explored within the context of pulmonary arterial hypertension (PAH). This study aims to identify genes implicated in PAH that are involved in disulfidptosis.
methodBased on data from the GEO database, this study employed co-expression analysis, Weighted Gene Co-Expression Network Analysis (WGCNA), hub gene identification, and Gene Set Enrichment Analysis (GSEA) to uncover genes associated with PAH and disulfidptosis. Subsequent machine learning validation and functional GSEA further refined the identification of pivotal genes. The investigation extended to examining immune cell involvement via immune infiltration techniques and elucidates the hub genes' roles within ceRNA networks.
resultThe integrative approach of co-expression analysis and WGCNA identified genes at the intersection of PAH and disulfidptosis. GSEA revealed their roles in essential biological processes and pathways, such as mRNA processing and cytoplasmic DNA sensing pathway. Prominently, USP32 and ZNF655 were identified as significant hub genes through machine learning analysis, demonstrating notable diagnostic potential across various datasets. Further, immune infiltration studies and ceRNA regulatory network construction revealed the intricate association between these genes and differential immune cell expression, alongside miRNA and lncRNA regulatory networks.
conclusionsThis study elucidates the contributory role of USP32 and ZNF655 in the pathogenesis of PAH, making them as critical genes within the disulfidptosis pathway.
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.