ArticleScientific reports2025
Identification of CTSK as a TLR-related critical biomarker in liver cirrhosis via integrative bioinformatics and pathological characterization.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Identification of potential biomarkers and therapeutic targets for liver cirrhosis based on Mendelian randomization and machine learning.Biochemistry and biophysics reports · 2026Article
- Cathepsin K Alleviates Liver Fibrosis by Inhibiting the TGF-β/Smad Signaling Pathway and Inducing Hepatic Stellate Cell Apoptosis.Journal of clinical and translational hepatology · 2026Article
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Authors and funding
14 authors.
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Abstract
Liver cirrhosis (LC) is a common chronic disease worldwide with a poor prognosis, and its pathogenesis has not been fully elucidated. Toll-like receptors (TLRs) are crucial in LC progression. Here, we identified TLR-related genes, providing novel insights related to LC diagnosis, pathogenesis, and treatment. Data from public databases were analyzed using "limma" and WGCNA to screen candidate genes, and four hub genes (CXCL9, CXCL10, SPP1, CTSK) were selected through machine learning. These hub genes were validated through bioinformatics, quantitative real-time PCR (qRT-PCR), and immunohistochemistry (IHC). Both the hub genes and risk models demonstrated strong diagnostic potential for LC. The hub genes were enriched in various pathways and strongly correlated with immune infiltration. Subtypes characterized by different TLR signaling activity exhibited distinct immune responses. scRNA-seq analysis revealed significant differences in hub gene expression and TLR signaling activity across different cell types. ceRNA network analysis revealed interactions involving miRNAs, lncRNAs, and hub genes. Molecular docking supported the potential value of the hub genes as drug targets. In conclusion, TLR-related hub genes exhibit excellent diagnostic and therapeutic value in LC, and their dysregulation contributes to immune disorders and activation of pathogenic signaling pathways. CTSK may stimulate the TLR4-MyD88-NF-κB axis to facilitate LC progression.
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