ArticleJournal of thrombosis and haemostasis : JTH2024
Enhanced venous thrombosis and hypercoagulability in murine and human metabolic dysfunction-associated steatohepatitis.
Article in Journal of thrombosis and haemostasis : JTH, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- From liver to cardiovascular system: the MASLD-ASCVD continuum.Internal and emergency medicine · 2026Review
- Neutrophil CD14 is a driver and a therapeutic target for deep vein thrombosis.Blood advances · 2026Article
- Sex-based multiomics analysis uncovers metabolic and molecular mediators linking MASH and atherosclerosis.JHEP reports : innovation in hepatology · 2026Article
- Direct oral anticoagulants in patients with advanced cirrhosis: is it time?Research and practice in thrombosis and haemostasis · 2026Article
- Clinical and pathophysiological perspectives on haemostasis, inflammation, and thrombo-haemorrhagic risk in cirrhosis.EXCLI journal · 2026Review
- Alcohol, Liver Disease, and Peripheral Arterial Disease: Epidemiology, Mechanisms, and Clinical Implications.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- EHBP1 suppresses liver fibrosis in metabolic dysfunction-associated steatohepatitis.Cell metabolism · 2025Article
- Design, Synthesis, and Biological Evaluation of Novel Hydroxytyrosol Derivatives as Protectors for Vascular Endothelium Against Lipid Overload.Drug design, development and therapy · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
backgroundPatients with metabolic dysfunction-associated steatohepatitis (MASH) are at an increased risk of developing venous thromboembolic events, including deep vein thrombosis (DVT). To date, the study of DVT in MASH has been hampered by the lack of reliable models that mimic the pathologic aspects of human disease.
objectivesTo evaluate DVT severity and hypercoagulability in murine and human MASH.
methodsTranscriptional changes in the liver, plasma markers of coagulation, and DVT severity were evaluated in mice fed a standard chow diet or a high-fructose, high-fat, and high-cholesterol MASH diet for 24 weeks. Plasma analyses of coagulation markers and thrombin generation assays were performed in a well-characterized cohort of patients with or without MASH.
resultsMice fed the MASH diet developed steatohepatitis and fibrosis, mimicking human MASH. Liver RNA sequencing revealed a significant upregulation of pathways related to inflammation and coagulation concomitant with increased levels of plasma coagulation markers including increased prothrombin fragment 1+2, thrombin-antithrombin complex, plasminogen activator inhibitor-1 levels, and endothelin 1. MASH exacerbated DVT severity in mice, as evidenced by increased thrombus weight and higher thrombosis incidence (15/15 vs 11/15 in controls, P = .0317). Higher endothelin 1 release and increased apoptosis were found in endothelial cells stimulated with supernatants of palmitate-stimulated HepG2 cells. Patients with MASH exhibited increased levels of plasma coagulation markers and delayed thrombin generation.
conclusionWe report enhanced DVT severity and hypercoagulability, both in murine and human MASH. Our model of MASH-DVT can facilitate a better understanding of the fundamental mechanisms leading to increased venous thromboembolic events in patients with MASH.
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