The widespread occurrence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to a pandemic of coronavirus disease 2019 (COVID-19). The S spike protein of SARS-CoV-2 binds with angiotensin-converting enzyme 2 (ACE2) as a functional “receptor” and then enters into host cells to replicate and damage host cells and organs. ACE2 plays a pivotal role in the inflammation, and its downregulation may aggravate COVID-19 via the renin-angiotensin system, including by promoting pathological changes in lung injury and involving inflammatory responses. Severe patients of COVID-19 often develop acute respiratory distress syndrome and multiple organ dysfunction/failure with high mortality that may be closely related to the hyper-proinflammatory status called the “cytokine storm.” Massive cytokines including interleukin-6, nuclear factor kappa B (NFκB), and tumor necrosis factor alpha (TNFα) released from SARS-CoV-2-infected macrophages and monocytes lead inflammation-derived injurious cascades causing multi-organ injury/failure. This review summarizes the current evidence and understanding of the underlying mechanisms of SARS-CoV-2, ACE2 and inflammation co-mediated multi-organ injury or failure in COVID-19 patients.

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 的广泛出现导致了 2019 年冠状病毒病 (COVID-19) 的大流行。SARS-CoV-2的S刺突蛋白作为功能性“受体”与血管紧张素转换酶2（ACE2）结合，然后进入宿主细胞复制并损伤宿主细胞和器官。ACE2在炎症中发挥着关键作用，其下调可能通过肾素-血管紧张素系统加重COVID-19，包括促进肺损伤的病理变化并涉及炎症反应。COVID-19的重症患者经常出现急性呼吸窘迫综合征和多器官功能障碍/衰竭，死亡率很高，这可能与被称为“细胞因子风暴”的过度促炎状态密切相关。SARS-CoV-2 感染的巨噬细胞和单核细胞释放的大量细胞因子，包括白细胞介素 6、核因子 kappa B (NFκB) 和肿瘤坏死因子 α (TNFα)，会导致炎症衍生的损伤性级联反应，导致多器官损伤/衰竭。本综述总结了对 SARS-CoV-2、ACE2 和炎症共同介导的 COVID-19 患者多器官损伤或衰竭的潜在机制的当前证据和理解。