ArticleNature communications2025
Hexokinase 2-mediated histone H3K18la promotes PAI-1-dependent thrombosis in acute myeloid leukemia via tumor-endothelial crosstalk.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Loss of MCT1 mediated lactate uptake causes delayed endplate maturation and intervertebral disc degeneration.Cell death & disease · 2026Article
- Lactate-lactylation in tumor angiogenesis and progression: mechanisms, biomarker potential, and therapeutic implications.Biomarker research · 2026Review
- Gut-derived small extracellular vesicles support trained innate immune tolerance in murine microglial cells.Frontiers in immunology · 2026Article
- Research progress on protein lactylation in female reproductive disease: molecular mechanisms, functions, and therapeutic implications.Frontiers in pharmacology · 2026Review
- Integrative profiling of lactylation reveals prognostic biomarkers and an immunosuppressive niche in acute myeloid leukemia.Frontiers in immunology · 2026Article
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Authors and funding
14 authors.
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Abstract
Acute myeloid leukemia is an aggressive hematological malignancy frequently complicated by coagulation disorders, including thrombosis and hemorrhage, which contribute to poor outcomes. Here, we identify lactate-driven histone lactylation as a mechanism promoting thrombosis in acute myeloid leukemia. We demonstrate that hexokinase 2-mediated glycolysis in leukemic cells leads to lactate accumulation, which enhances histone H3 lysine 18 lactylation and upregulates plasminogen activator inhibitor-1 expression, impairing fibrinolysis. Lactate released by acute myeloid leukemia cells is internalized by vascular endothelial cells via monocarboxylate transporter 1, amplifying plasminogen activator inhibitor-1 expression and thrombotic risk. Inhibition of hexokinase 2-mediated lactate production or monocarboxylate transporter 1-mediated lactate uptake attenuates thrombosis. Our findings reveal a critical link between tumor metabolism, epigenetic modifications, and coagulation dysfunction in acute myeloid leukemia.
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