ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2026
Multi-omics investigation into the role of PTK7 as a driver of liver fibrosis.
Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesLiver fibrosis is a critical stage in the progression of chronic liver disease to cirrhosis, and effective antifibrotic targets remain lacking. This study aims to investigate the association between protein tyrosine kinase 7 (PTK7) and liver fibrosis through multi-omics analyses, explore its potential role in hepatic stellate cell activation, and evaluate the value of circulating PTK7 as a candidate biomarker for assessing liver fibrosis severity.
methodsGenome-wide association study (GWAS) summary statistics, cis-expression quantitative trait locus (cis-eQTL), and plasma protein quantitative trait locus (pQTL) datasets were integrated to identify candidate genes associated with liver fibrosis. Candidate genes were further validated using multiple machine-learning models in three independent Gene Expression Omnibus (GEO) cohorts (GSE84044, GSE25097, and GSE49541). Human and murine liver single-cell transcriptomic datasets were analyzed to characterize the expression profile of PTK7. In an exploratory clinical cohort, plasma PTK7 levels were measured by enzyme-linked immunosorbent assay (ELISA), and PTK7 expression was evaluated in a carbon tetrachloride (CCl
resultsA total of 18 candidate genes were identified, among which PTK7 consistently showed upregulated expression in fibrotic liver tissues across multiple datasets. Single-cell transcriptomic analysis revealed enriched PTK7 expression in Kupffer cells and fibroblast-related populations. Plasma PTK7 levels were significantly elevated in patients with liver fibrosis and were positively correlated with liver stiffness measurements. In activated LX-2 cells, PTK7 knockdown reduced the expression levels of collagen type I alpha 1 chain (COL1A1), alpha-smooth muscle actin (α-SMA), and β-catenin. Furthermore, rescue experiments using SKL2001 supported the involvement of β-catenin-related signaling pathways in PTK7-mediated profibrotic effects. Computational analyses suggested a stable interaction pattern between PTK7 and β-catenin.
conclusionsPTK7 is closely associated with liver fibrosis at both multi-omics and transcriptomic levels, may participate in hepatic stellate cell activation, and may be associated with β-catenin-related signaling pathways. Circulating PTK7 may serve as a candidate biomarker for reflecting the severity of liver fibrosis; however, further validation in larger clinical cohorts is warranted.
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