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Fig. 3 | Critical Care

Fig. 3

From: The impact of acquired coagulation factor XIII deficiency in traumatic bleeding and wound healing

Fig. 3

The roles of plasma FXIII (pFXIII) during wound healing. a Following injury and leakage of blood constituents into the wound, pFXIII enhances aggregation of platelets to the injured endothelium, limiting exudation. b Activated pFXIII (pFXIIIa) mediates cross-linking of the deposited fibrin, structural macromolecules, fibrinolytic inhibitors, and invading pathogens. c, d Inflammatory mediators secreted by, for example, platelets and epithelium lead to recruitment of neutrophils, monocytes and additional leukocytes into the wound. FXIIIa-induced cross-linking of the provisional matrix creates the basis for their integrin-mediated interactions with the provisional matrix. This enhances cellular invasion of the wound, and stimulates leukocyte survival and proliferation. e During granulation tissue formation, fibroblasts and endothelial cells (ECs) invade the wound, facilitating collagen deposition and angiogenesis. They are guided through integrin interactions with cross-linked macromolecules in the wound, and this stimulates their migration and survival. FXIIIa stimulates angiogenesis and granulation tissue formation by mediating complex formation of endothelial αVβ3 and vascular endothelial growth factor receptor 2 on ECs. f Through the ongoing remodelling phase, the normal tissue architecture is re-established. IL, interleukin; PAI-2, plasminogen activator inhibitor-2; PDGF, platelet-derived growth factor; TAFI, thrombin-activatable fibrinolysis inhibitor; TGF-b, transforming growth factor-b; VWF, von Willebrand factor. From [9], ©2013 International Society on Thrombosis and Haemostasis. Reprinted with permission)

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