Author

Zixin Pi

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Open access Jul 2026

Integrated Bioinformatics Analysis Reveals Candidate Hub Genes and Regulatory Networks Associated with Preeclampsia

Preeclampsia (PE) is a severe pregnancy-associated hypertensive disorder and a major contributor to maternal and perinatal morbidity and mortality. The mechanisms of PE pathogenesis are not yet understood. This paper aims to explore candidate PE-associated biomarkers and regulatory mechanisms using bioinformatics analysis of placental transcriptomic datasets. We downloaded placental transcriptomic datasetsGSE203507 and GSE148241 from GEO and investigated differentially expressed genes(DEGs) between PE and control samples. We performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Disease Ontology (DO), and protein–protein interaction (PPI) analyses to characterize the potential role, disease associations, and interaction networks of the DEGs. We validated the mRNA expression patterns of candidate hub genes using two independent placental transcriptomic datasets, GSE143966 and GSE114691.We identified 263 DEGs in the discovery analysis and further obtained 150 overlapping DEGs including80 upregulated genes and 70 downregulated genes, for downstream analysis. We then identified eight candidate hub genes: OPRK1, OXGR1, HCAR3, CCR5, HCAR2, CXCL1, FPR3, and SSTR1using Meta scape software(v3.5.20260201). In the validation phase, most candidate hub genes showed broadly consistent mRNA expression trends across GSE114691 and GSE143966, while FPR3 showed weaker cross-dataset consistency. These findings provide candidate PE-associated genes and regulatory pathways for further experimental and clinical validation..

Dan Jiang, Haiyan Xiong, Qingqing Li et al. · bioRxiv · 0 citations

Aug 2026

A novel LncRNA TUG1/miR-30d/e-3p/SNAI2 ceRNA axis drives dermal fibrosis in systemic sclerosis via direct transcriptional activation of COL1A1.

Systemic sclerosis (SSc) is a severe autoimmune disease characterized by progressive dermal fibrosis, aberrant fibroblast activation, and excessive collagen deposition. Although noncoding RNA-mediated regulation has been increasingly implicated in fibrotic diseases, the role of the long noncoding RNA taurine-upregulated gene 1 (TUG1) in SSc-associated skin fibrosis remains unclear. In this study, we investigated the function and mechanism of TUG1 in primary dermal fibroblasts isolated from lesional skin of patients with SSc and in a bleomycin-induced mouse model of dermal fibrosis. TUG1 expression was significantly increased in SSc dermal fibroblasts. Functional assays showed that TUG1 promoted fibroblast proliferation, migration, and COL1A1 expression, whereas TUG1 silencing attenuated these profibrotic phenotypes. Mechanistically, TUG1 acted as a competing endogenous RNA by sponging miR-30d-3p and miR-30e-3p, thereby relieving their repression of the transcription factor SNAI2. SNAI2 directly bound to the COL1A1 promoter and activated its transcription. In vivo, Tug1 knockdown alleviated bleomycin-induced dermal fibrosis, increased miR-30d-3p/miR-30e-3p levels, and reduced SNAI2 expression and collagen deposition. These findings identify the TUG1-miR-30d-3p/miR-30e-3p-SNAI2-COL1A1 axis as a potential therapeutic target in SSc skin fibrosis.

Ruixuan Zhu, Yangfan Xiao, Licong Liu et al. · International Immunopharmaco... · 0 citations