ArticleJournal of thoracic disease2023
Bioinformatics and functional experiments reveal that
Article in Journal of thoracic disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Integrated bioinformatics and network search identify biomarkers and comorbid mechanisms of atrial fibrillation and ischemic stroke.Medicine · 2026Article
- HSPD1 regulates angiotensin II‑induced atrial fibrillation via the PPAR signaling pathway.Molecular medicine reports · 2025Article
- Macrophage MRC2 deficiency mitigates HFD-induced MASLD by downregulating CD147-regulated TNF-α production.JHEP reports : innovation in hepatology · 2025Article
- Epigenome-wide association study of perceived discrimination in the Multi-Ethnic Study of Atherosclerosis (MESA).Epigenetics · 2025Article
- Multiomic and electrophysiologic analyses reveal that an inherited MRC2 variant causes fibroblast dysfunction and increased atrial fibrillation susceptibility.American journal of physiology. Heart and circulatory physiology · 2025Article
- Rare Variant inCirculation. Genomic and precision medicine · 2024Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atrial fibrillation (AF) is a prevalent cardiac arrhythmia that requires improved clinical markers to increase diagnostic accuracy and provide insight into its pathogenesis. Although some biomarkers are available, new ones need to be discovered to better capture the complex physiology of AF. However, their limitations are still not fully addressed. Bioinformatics and functional studies can help find new clinical markers and improve the understanding of AF, meeting the need for early diagnosis and individualized treatment. Methods: To identify AF-related differentially expressed genes (DEGs), We applied the messenger RNA (mRNA) expression profile retrieved in Series Matrix File format from the GSE143924 microarray dataset obtained from the Gene Expression Omnibus (GEO) database, and then used weighted gene co-expression network analysis (WGCNA) to identify the overlapping genes. These genes were analyzed by enrichment analysis, expression analysis and others to obtain the hub gene. Additionally, the potential signaling pathway of hub gene in AF was explored and verified by functional experiments, like quantitative real-time polymerase chain reaction (qRT-PCR), cell counting kit-8 (CCK-8), flow cytometry, and Western blotting (WB) assay. Results: From the GSE143924 data (410 DEGs) and tan module (57 genes), 10 overlapping genes were identified. A central down-regulated gene in AF, Conclusions: While meeting the need for new biomarkers in the diagnosis and prognosis of AF, this study reveals the inherent limitations of current biomarkers. We identified
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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.