Department of Clinical, Internal, Anesthesiological, and Cardiovascular Sciences, University of Rome 'Sapienza', Italy.
University College of Dublin, Mater Misericordiae University Hospital, Dublin, Republic of Ireland.
J Cardiovasc Med (Hagerstown). 2020 Sep;21(9):630-633. doi: 10.2459/JCM.0000000000001071.
: 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.
血管紧张素转换酶 2(ACE2)受体在细胞膜中有广泛的表达模式,对心血管疾病的发展具有保护作用。最近,这种酶在 COVID-19(2019 年冠状病毒病)大流行感染期间引起了极大的关注。该病毒通过 ACE2 作为跨膜受体入侵肺泡上皮细胞和心肌细胞。ACE2 是一种对抗调节肽,可将血管紧张素 II(Ang II)降解为 Ang 1-7,从而减弱 AT1 受体的生物学效应。COVID-19 的刺突蛋白与该酶之间的结合对于病毒进入靶细胞至关重要,但 ACE2 活性的增加是否会促进感染尚未得到证实。然而,这一方面引发了人们对感染患者或有感染风险患者使用 ACE 抑制剂或 ARB 的诸多担忧。似乎细胞感染会导致 ACE2 表达减少和 Ang II--AT1 轴活性增加,从而导致促炎细胞因子释放、ARDS、心肌炎和高凝状态,有可能使急性冠状动脉综合征恶化、诱发肺栓塞或出现弥散性血管内凝血。因此,感染患者应继续使用 ACE 抑制剂或血管紧张素受体阻滞剂药物,因为它们的停用会增加 Ang II 活性并导致肺部或心血管系统损伤。