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. 2022 Feb 3;42(3):261–276. doi: 10.1161/ATVBAHA.121.316930

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© 2022 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 2. — Neutrophil extracellular traps (NETs) promote fibrin formation by interacting with the coagulation system. NETs stimulate the formation of fibrin by triggering both the extrinsic (TF [tissue factor]) as well as intrinsic (FXII) pathway of the coagulation system (green arrows). In addition, histones are able to prevent the cleavage of FVa by APC (activated protein C). By the autoactivation of prothrombin or the interaction with TLR2 or 4 (toll-like receptor 2 or 4) on platelets, histones directly trigger thrombin generation (green arrows). Besides directly stimulating fibrin formation, NETs prevent its degradation by impairing t-PA (tissue-type plasminogen activator), u-PA (urokinase-type plasminogen activator), antithrombin, and plasmin-mediated lysis (green arrows). Not only are NETs able to interact with various components of the coagulation cascade, but these components (FXII and thrombin) can also prime for NETosis (blue arrows). UPAR indicates urokinase-type plasminogen activator receptor.