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Figure 2 | Critical Care

Figure 2

From: Clinical review: Molecular mechanisms underlying the role of antithrombin in sepsis

Figure 2

Inflammation-modulating effect of antithrombin on the endothelium. Ligation of heparan sulfate proteoglycans (HSPGs) of endothelium with antithrombin (AT) induces cellular signalling events that alter the cell's biochemical and functional responses to inflammatory stimuli (e.g. bacterial lipopolysaccharide [LPS]). Changes include reduced release of inflammatory and procoagulatory mediators (e.g. interleukin [IL]-1, IL-6, tumour necrosis factor-α[TNF]), tissue factor (TF), adenosine diphosphate (ADP) and cellular adhesion molecules (not shown), as well as increased release of anticoagulatory prostacyclin (prostaglandin [PG]I) or CD39/ATPDase. In neuronal tissue, protective mechanisms may by mediated via the release of calcitonin gene-related peptide and nitric oxide with the potential to affect prostacyclin release [55].

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