COVID-19-associated coagulopathy (CAC) is a life-threatening complication of SARS-CoV-2 infection. However, the underlying cellular and molecular mechanisms driving this condition are unclear. Evidence supports the concept that CAC involves complex interactions between the innate immune response, the coagulation and fibrinolytic pathways, and the vascular endothelium, resulting in a procoagulant condition. Understanding of the pathogenesis of this condition at the genomic, molecular and cellular levels is needed in order to mitigate thrombosis formation in at-risk patients. In this Perspective, we categorize our current understanding of CAC into three main pathological mechanisms: first, vascular endothelial cell dysfunction; second, a hyper-inflammatory immune response; and last, hypercoagulability. Furthermore, we pose key questions and identify research gaps that need to be addressed to better understand CAC, facilitate improved diagnostics and aid in therapeutic development. Finally, we consider the suitability of different animal models to study CAC.

COVID-19 相关凝血病 (CAC) 是 SARS-CoV-2 感染的一种危及生命的并发症。然而，驱动这种情况的潜在细胞和分子机制尚不清楚。有证据支持这一概念，即 CAC 涉及先天免疫反应、凝血和纤溶途径以及血管内皮之间复杂的相互作用，从而导致促凝血状态。为了减轻高危患者的血栓形成，需要在基因组、分子和细胞水平上了解这种疾病的发病机制。在本篇文章中，我们将目前对CAC的认识分为三个主要病理机制：一是血管内皮细胞功能障碍；二是血管内皮细胞功能障碍。第二，高炎症免疫反应；最后，高凝状态。此外，我们提出了关键问题并确定了需要解决的研究差距，以更好地了解 CAC、促进改进诊断并帮助治疗开发。最后，我们考虑不同动物模型研究 CAC 的适用性。