Coronavirus disease 2019 (COVID‐19) pathogenesis remains under investigation. Growing evidence indicates the establishment of a hyperinflammatory response, characterized by sustained production of cytokines, such as IL‐1β. The release and maturation of this cytokine are dependent on the activation of a catalytic multiprotein complex, known as “inflammasome”. The most investigated is the NLRP3 inflammasome, which can be activated by various stimuli, such as the recognition of extracellular ATP by the P2X7 receptor. Based on the recent literature, we present evidence that supports the idea that the P2X7R/NLRP3 axis may be involved in the immune dysregulation caused by the SARS‐CoV‐2 infection.

中文翻译：

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P2X7 受体在 COVID-19 发病机制中的潜在参与：新的治疗靶点？


2019 年冠状病毒病 (COVID-19) 的发病机制仍在研究中。越来越多的证据表明过度炎症反应的建立，其特征是持续产生细胞因子，例如 IL-1β。这种细胞因子的释放和成熟取决于催化多蛋白复合物（称为“炎症小体”）的激活。研究最多的是NLRP3炎症小体，它可以被各种刺激激活，例如P2X7受体对细胞外ATP的识别。根据最近的文献，我们提供的证据支持以下观点：P2X7R/NLRP3 轴可能参与 SARS-CoV-2 感染引起的免疫失调。