ArticleHereditas2025
Exploring the potential mechanisms of m6A modification in septic acute respiratory distress syndrome: a bioinformatics analysis.
Article in Hereditas, 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
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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.
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Who cites it
1 citing paper in PubMed.
- The regulation of oxidative stress response by epigenetic modifications in acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundAcute respiratory distress syndrome (ARDS) remains a leading cause of mortality in intensive care units. The N6-methyladenosine (m6A) mRNA modification is critical in various pathological conditions, yet its role in the ARDS microenvironment, particularly at the single-cell level, remains poorly understood.
methodsSingle-cell and bulk RNA-sequencing datasets were sourced from the GEO databases. Bioinformatics and experimental approaches were employed to investigate the associations between m6A regulators and hub genes in ARDS.
resultsWTAP, HNRNPA2B1, and HNRNPC exhibited extensive expression within the ARDS microenvironment. Consensus clustering analysis segregated patients with sepsis into distinct subgroups, with WTAP showing significant variation across these groups. Weighted gene co-expression network analysis (WGCNA) identified the brown module as most associated with WTAP, revealing five hub genes. Validation experiments confirmed high expression levels of WTAP and MYC in lung tissues. Functional assays further demonstrated that WTAP enhances ARDS progression.
conclusionsIn conclusion, bioinformatics analysis and preliminary experimental data suggest that WTAP promotes ARDS onset and progression by regulating m6A methylation and facilitating immune cell infiltration.
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