Extracellular Vesicles Reflect Thrombo‐Inflammatory, Endothelial and Tissue‐Remodelling Changes in Cirrhosis

作者：Elena Campello, Alberto Zanetto, Kymentie Ferdinande, S. Toffanin, Cristiana Bulato, Claudia Radu, Chiara Samà, Luca Spiezia, F P Russo, Patrizia Burra, Marco Senzolo, Paolo Simioni · 发表于：Liver International · 年份：2026 · DOI：10.1111/liv.70723 · 被引用次数：1 · 研究领域：Extracellular vesicles in disease、interferon and immune responses、Liver Disease and Transplantation

BACKGROUND AND AIMS: Cirrhosis is characterized by progressive immune dysregulation, endothelial dysfunction, and haemostatic imbalance. Circulating extracellular vesicles (EVs) have emerged as potential biomarkers reflecting these pathophysiological processes. We aimed to determine whether EVs mirror disease severity and predict liver-related outcomes in cirrhosis. METHODS: EVs, EVs expressing markers associated with endothelial anticoagulant pathways and tissue remodelling. Primary endpoints were first hepatic decompensation in compensated cirrhosis and a composite of further decompensation, acute-on-chronic liver failure, or liver-related mortality in acutely decompensated cirrhosis. Associations were analysed using Fine-Grey competing-risk models. RESULTS: We included 228 patients, including 75 compensated, 44 stable decompensated, and 109 acutely decompensated. Median follow-up was 418 days. EV profiling showed progressive increases in total, platelet-derived, endothelial-, immune-derived, and tissue remodelling-associated EVs across Child-Pugh stages, suggestive of increasing thrombo-inflammatory and endothelial perturbation. First hepatic decompensation occurred in 7 patients with compensated cirrhosis and was associated with higher MELD and Child-Pugh scores, alcohol-related aetiology, and lower platelet count. In univariate competing-risk analyses, higher levels of several EV subpopulations were associated with first decompensation, but these associations disappeared...