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. 2021 Jan 28;3(1):3–12. doi: 10.2991/chi.k.210117.001

Figure 1.

Figure 1

Pathogenesis of CRS-related coagulopathy. (a) Pro-inflammatory cytokines IL-1, IL-6 and TNF-α can stimulate endothelial cells (ECs) to secrete Weibel–Palade (W–P) body, which contains ultra-large von Willebrand factor (UL-vWF) and P-selection; both are essential for platelet attachment. Moreover, the cytoskeletons of ECs are rearranged to expose the procoagulant collagen. The expressions of anticoagulant proteins such as the endothelial protein C receptors (EPCR) and ADAMTS-13 are also downregulated. (b) Cytokines IL-1, IL-6, TNF-α and IFN-γ can affect the quantity and quality of platelets. The megakaryocyte maturation is accelerated resulting in more platelets. These cytokines can also stimulate the release of dense granules and α-granules, which contain essential coagulation substrates such as the fibrinogen and vWF. (c) Cytokines IL-1, IL-6, and TNF-α can increase the expression of tissue factor from ECs and on monocytes. In addition, the fibrinolytic system is inhibited with increased expression of plasminogen activator inhibitor type I (PAI-1), which can deactivate tPA and result in less plasmin. ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; IFN, interferon; tPA, tissue plasminogen activator.