Pluripotent mechanisms for regulation of hemostasis and thrombogenesis in COVID‐19: 612.115.3

Abstract

Summary. Severe conditions in patients with COVID‐19 are associated with severe hypercoagulability, which leads to thromboembolic complications and multiple organ failure as the main cause of death. At the same time, along with the classical pathway, the causative agent of COVID‐19, SARS‐CoV‐2 coronavirus, leads to the development of so‐called alternative pathways for the mechanisms of blood coagulation and fibrinolysis. Alternative pathways for the development and regulation of hemostasis and thrombogenesis are associated with the impact of the spike protein S (PROS1) and papain‐like protease (PLpro) of SARS‐CoV‐2 coronavirus, the action of complement fragments and the membrane attack complex, and the activation of renin‐angiotensinaldosterone and kallikrein‐kinin systems, hyperstimulation of the immune response leading to a cytokine storm, the influence of mannose‐binding lectin‐associated serine proteases (MASPs), activated neutrophils with the formation of neutrophil extracellular traps (NЕTs), microvesicles of various origins, the influence of an increased concentration of tryptases, mainly trypsin and others, so far little studied factors. Successful therapy of serious COVID‐19‐patients and prevention of thrombosis requires the elimination of the cytokine storm, which can be largely achieved by using cytokine inhibitors or thymus peptides (thymalin) as immunocorrectors, as well as anti‐SARS‐CoV‐2 matrix antibodies. Due to the “proteolytic explosion” alpha‐1‐antitrypsin or other antiprotease drugs should be used in serious COVID‐19 patients. Alternative hemostatic mechanisms are suggested to develop not only in COVID‐19, but also in other diseases and even in normal conditions, but their effect on blood coagulation and fibrinolysis are small.

For citation: Kuznik B.I., Roitman E.V., Tsybikov N.N., Shapovalov K.G., Smolyakov Yu.N. Pluripotent mechanisms for regulation of hemostasis and thrombogenesis in COVID‐19. Tromboz, gemostaz i reologiya. 2023;(2):67–89.

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