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Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis
Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis
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Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis
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Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis
Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis

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Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis
Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis
Journal Article

Several implications for the pathogenesis and treatment of thrombosis in PNH patients according to multiomics analysis

2024
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Overview
Through Augur analysis, we found that myeloid cells, including neutrophils, myelocytes and monocytes, contributed significantly to the thrombotic phenotype (Fig. 1D). [...]we analyzed the DEGs of myeloid cells and found that genes related to leukocyte activation, adhesion and migration to the endothelium were upregulated, while genes related to leukocyte-mediated immunity and cell killing were downregulated (Fig. 1E, F). Enrichment analysis shows that the differentially expressed proteins (DEPs) are involved in cell adhesion, platelet activation, fibrinogen complex, and complement and coagulation cascade (Fig. 1H, Additional file 1: [...]we demonstrate that platelet activation, coagulation cascades, and leukocyte cell adhesion are closely related to thrombosis in PNH patients at multiple levels of gene, transcription, and protein.