LGALS3BP in liver cirrhosis: a genetic-based discovery from platelet-related genes with predictive diagnostic value

Background Thrombocytopenia, a major complication of liver cirrhosis, elevates bleeding risk and worsens patient prognosis, especially after invasive procedures. Despite its clinical significance, the molecular mechanisms underpinning platelet dysfunction in cirrhosis remain elusive. Methods We conducted an integrative analysis to define the diagnostic value of platelet-related genes in cirrhosis and to decipher platelet-liver cell interactions. Bioinformatics approaches were applied to public datasets to identify key genes and construct a receiver operating characteristic (ROC)-based diagnostic model, with validation in multiple independent cohorts. Functional enrichment and immune infiltration analyses were performed. Findings were experimentally validated using qRT-PCR and immunohistochemistry in clinical samples. Results We established a robust platelet-related gene diagnostic model and identified LGALS3BP as a high-value diagnostic biomarker for liver cirrhosis. Groups with high and low LGALS3BP expression exhibited distinct biological functions and immune microenvironment profiles, suggesting an immunomodulatory role in disease progression. Crucially, in vitro functional studies demonstrated that LGALS3BP acts as a key molecular mediator linking hepatic fibrosis to platelet activation. Conclusion This study identifies LGALS3BP as a pivotal molecular link in cirrhotic thrombocytopenia and establishes a novel diagnostic model based on platelet-related genes. Our findings highlight LGALS3BP's role in mediating platelet-liver cell crosstalk and its association with the immune microenvironment, providing new insights into disease progression. This work not only advances the molecular understanding of liver cirrhosis but also offers a promising diagnostic tool with potential clinical utility.