Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.
Department of Medical Biotechnology, Faculty of Biophysics, Biochemistry and Biotechnology, Jagiellonian University, 30-387 Krakow, Poland.
Int J Mol Sci. 2023 Jan 27;24(3):2492. doi: 10.3390/ijms24032492.
Platelet-endothelial interactions have a critical role in microcirculatory function, which maintains tissue homeostasis. The subtle equilibrium between platelets and the vessel wall is disturbed by the coronavirus disease 2019 (COVID-19), which affects all three components of Virchow's triad (endothelial injury, stasis and a hypercoagulable state). Endotheliitis, vasculitis, glycocalyx degradation, alterations in blood flow and viscosity, neutrophil extracellular trap formation and microparticle shedding are only few pathomechanisms contributing to endothelial damage and microthrombosis resulting in capillary plugging and tissue ischemia. In the following opinion paper, we discuss major pathological processes leading to microvascular endothelial activation and thrombosis formation as a possible major adverse factor driving the deterioration of patient disease course in severe COVID-19.
血小板-内皮细胞相互作用在维持组织稳态的微循环功能中起着关键作用。新型冠状病毒病 2019（COVID-19）破坏了这种微妙的平衡，影响了Virchow 三联征的所有三个组成部分（内皮损伤、停滞和高凝状态）。内皮炎、血管炎、糖萼降解、血流和粘度改变、中性粒细胞胞外诱捕网形成和微粒体脱落只是导致内皮损伤和微血栓形成的部分病理机制，导致毛细血管堵塞和组织缺血。在这篇专题讨论文章中，我们讨论了导致微血管内皮激活和血栓形成的主要病理过程，这可能是严重 COVID-19 患者病情恶化的一个主要不利因素。
