ACE2 receptor has a broad expression pattern in the cellular membrane and provides a protective action against the development of cardiovascular diseases. Recently, this enzyme has become of extreme interest during the pandemic infection of COVID-19 (coronavirus disease 2019). This virus invades alveolar epithelium and cardiomyocytes using ACE2 as a transmembrane receptor. ACE2 is a counter-regulatory peptide that degrades Ang II into Ang 1–7, thereby attenuating the biological effects of the AT1 receptor. The binding between the spike protein of COVID-19 and the enzyme is crucial for the virus to enter the target cells, but whether an increase in ACE2 activity could facilitate the infection is not yet demonstrated. However, this aspect has raised many concerns about the use of ACE inhibitors or ARBs in infected patients or patients at risk of infection. It appears that cellular infection leads to a reduction in ACE2 expression and an increase in the activity of the Ang II--AT1 axis, which leads to the release of pro-inflammatory cytokines, ARDS, myocarditis, and hypercoagulability with the possibility of exacerbation of acute coronary syndrome, induction of pulmonary embolism, or appearance of disseminated intravascular coagulation. Therefore, ACE inhibitors or angiotensin receptor blocker drugs should be continued in infected patients, as their discontinuation can increase Ang II activity and induce injury to the lungs or cardiovascular system.

ACE2受体在细胞膜中具有广泛的表达模式，并提供了针对心血管疾病发展的保护作用。最近，在大流行感染COVID-19（冠状病毒）过程中，这种酶已引起极大关注。疾病2019）。该病毒使用ACE2作为跨膜受体侵入肺泡上皮和心肌细胞。ACE2是一种反调节肽，可将Ang II降解为Ang 1-7，从而减弱AT1受体的生物学作用。COVID-19的突突蛋白与酶之间的结合对于病毒进入靶细胞至关重要，但是尚不能证明ACE2活性的增加是否可以促进感染。然而，这方面引起了许多关于在感染的患者或有感染风险的患者中使用ACE抑制剂或ARB的担忧。看来细胞感染导致ACE2表达降低，Ang II-AT1轴活性增加，从而导致促炎性细胞因子，ARDS，心肌炎，和高凝性，可能加重急性冠状动脉综合征，诱发肺栓塞或出现弥散性血管内凝血。因此，在感染的患者中应继续使用ACE抑制剂或血管紧张素受体阻滞剂，因为停用它们会增加Ang II活性并引起肺或心血管系统损伤。