ACE2 has emerged as a double agent in the COVID-19 ordeal, as it is both physiologically protective and virally conducive. The identification of ACE2 in as many as 72 tissues suggests that extrapulmonary invasion and damage is likely, which indeed has already been demonstrated by cardiovascular and gastrointestinal symptoms. On the other hand, identifying ACE2 dysregulation in patients with comorbidities may offer insight as to why COVID-19 symptoms are often more severe in these individuals. This may be attributed to a pre-existing proinflammatory state that is further propelled with the cytokine storm induced by SARS-CoV-2 infection or the loss of functional ACE2 expression as a result of viral internalization. Here, we aim to characterize the distribution and role of ACE2 in various organs to highlight the scope of damage that may arise upon SARS-CoV-2 invasion. Furthermore, by examining the disruption of ACE2 in several comorbid diseases, we offer insight into potential causes of increased severity of COVID-19 symptoms in certain individuals.

中文翻译：

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在合并症中血管紧张素转换酶2的表达和功能异常可能导致冠状病毒感染性疾病2019并发症的严重性

ACE2在COVID-19折磨中已成为一种双重药物，因为它既具有生理保护性又具有病毒学意义。在多达72个组织中鉴定出ACE2，表明可能发生肺外侵袭和破坏，而心血管和胃肠道症状的确已经证明了这一点。另一方面，在合并症患者中识别ACE2失调可能提供洞悉，为什么这些患者中COVID-19症状通常更严重。这可能归因于先前存在的促炎状态，这种状态进一步被SARS-CoV-2感染诱导的细胞因子风暴或由于病毒内在化而导致的功能性ACE2表达丧失所推动。这里，我们旨在表征ACE2在各种器官中的分布和作用，以突出SARS-CoV-2入侵可能引起的破坏范围。此外，通过检查几种合并症中ACE2的破坏，我们提供了对某些个体中COVID-19症状严重程度升高的潜在原因的见解。