FIGURE 1.

Schematic summary indicating the proposed pathophysiology underlying the role of NETosis in thrombosis. damage‐associated molecular patterns (DAMPs), platelets, and complement receptor engagement trigger nonlytic neutrophil extracellular trap (NET) formation, allowing NETing neutrophils to retain basic phagocytic and chemotactic functions. Nonlytic NETosis directly activates PAD‐4, which converts arginine to citrulline on histones, causing loss of positive charges of histones and disrupting electrostatic attractions between histones and DNA. The result is decondensation of chromatin. Subsequently, chromatin and associated proteins are lost via blebbing of the nuclear envelope, which is resealed afterward. NETs provide a structural basis for thrombosis and promote platelet aggregation and coagulation, manifesting as a pro‐thrombogenic state. Additionally, NETs can lead to the production of ANCA, leading to ANCA‐associated vasculitis which has been noted in severe cases of COVID‐19