ArticleRespiratory research2024
Identification of TFRC as a biomarker for pulmonary arterial hypertension based on bioinformatics and experimental verification.
Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- TRDMT1 slows lung cancer growth by stabilizing TFRC mRNA and triggering ferroptosis cell death.The Journal of biological chemistry · 2026Article
- Mechanistic studies of molecular networks associated with pulmonary hypertension explored by combined transcriptome analysis of Project-methylation.Clinical epigenetics · 2026Article
- Unveiling the role of Jagged2 in hypoxic pulmonary arterial hypertension: A NOX2-mediated pathway.Journal of cell communication and signaling · 2025Article
- Decoding the anti-hypertensive mechanism of α-mangostin based on network pharmacology, molecular docking and experimental validation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Prognostic and predictive value of pathohistological features in gastric cancer and identification of SLITRK4 as a potential biomarker for gastric cancer.Scientific reports · 2024Article
- A comprehensive analysis of genes associated with hypoxia and cuproptosis in pulmonary arterial hypertension using machine learning methods and immune infiltration analysis:Frontiers in medicine · 2024Article
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Abstract
backgroundPulmonary arterial hypertension (PAH) is a life-threatening chronic cardiopulmonary disease. However, there is a paucity of studies that reflect the available biomarkers from separate gene expression profiles in PAH.
methodsThe GSE131793 and GSE113439 datasets were combined for subsequent analyses, and batch effects were removed. Bioinformatic analysis was then performed to identify differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) and a protein-protein interaction (PPI) network analysis were then used to further filter the hub genes. Functional enrichment analysis of the intersection genes was performed using Gene Ontology (GO), Disease Ontology (DO), Kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA). The expression level and diagnostic value of hub gene expression in pulmonary arterial hypertension (PAH) patients were also analyzed in the validation datasets GSE53408 and GSE22356. In addition, target gene expression was validated in the lungs of a monocrotaline (MCT)-induced pulmonary hypertension (PH) rat model and in the serum of PAH patients.
resultsA total of 914 differentially expressed genes (DEGs) were identified, with 722 upregulated and 192 downregulated genes. The key module relevant to PAH was selected using WGCNA. By combining the DEGs and the key module of WGCNA, 807 genes were selected. Furthermore, protein-protein interaction (PPI) network analysis identified HSP90AA1, CD8A, HIF1A, CXCL8, EPRS1, POLR2B, TFRC, and PTGS2 as hub genes. The GSE53408 and GSE22356 datasets were used to evaluate the expression of TFRC, which also showed robust diagnostic value. According to GSEA enrichment analysis, PAH-relevant biological functions and pathways were enriched in patients with high TFRC levels. Furthermore, TFRC expression was found to be upregulated in the lung tissues of our experimental PH rat model compared to those of the controls, and the same conclusion was reached in the serum of the PAH patients.
conclusionsAccording to our bioinformatics analysis, the observed increase of TFRC in the lung tissue of human PAH patients, as indicated by transcriptomic data, is consistent with the alterations observed in PAH patients and rodent models. These data suggest that TFRC may serve as a potential biomarker for PAH.
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