Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target

By Haibo Zhang, Josef M. Penninger, Yimin Li, N. Zhong, Arthur S Slutsky. Intensive Care Medicine, 2020

2,157 citations recorded by the source corpus.

A novel infectious disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was detected in Wuhan, China, in December 2019. The disease (COVID-19) spread rapidly, reaching epidemic proportions in China, and has been found in 27 other countries. As of February 27, 2020, over 82,000 cases of COVID-19 were reported, with > 2800 deaths. No specific therapeutics are available, and current management includes travel restrictions, patient isolation, and supportive medical care. There are a number of pharmaceuticals already being tested [1, 2], but a better understanding of the underlying pathobiology is required. In this context, this article will briefly review the rationale for angiotensin-converting enzyme 2 (ACE2) receptor as a specific target.

Subfields: Computational Theory and Mathematics, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/344691fefbffe0d2b26a5e721f68e011121cd883

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In Computational Theory and Mathematics

Gisbert Schneider

In Infectious Diseases

Citations in the corpus

Inhibition of SARS-CoV-2 Infections in Engineered Human Tissues Using Clinical-Grade Soluble Human ACE2 (2020, positive): “Pathology due to SARS, MERS, and now COVID-19 is not limited to the lung; damage can occur in multiple organs (Gu et ACE2 is expressed in various tissues including the heart, kidney tubules, the luminal surface of the small intestine, and blood vessels (Crackower et al., 2002; Danilczyk and Penninge”
Intensive care management of coronavirus disease 2019 (COVID-19): challenges and recommendations (2020, neutral): “50,51 A conservative or de-resuscitative fluid strategy, 52 with early detection of myocardial involvement through the measurement of troponin and beta-natriuretic peptide concentrations and echocardiography, 53,54 and early use of vasopressors and inotropes are recommended (figure 2).”
COVID-19 and Cardiovascular Disease (2020, background): “inspired oxygen ratio <300, and/or lung infiltrates >50% within 24 to 48 hours) and 5% were critical (respiratory failure, septic shock, and/or multiple organ dysfunction or failure).(9) D ow nladed from http://journals.”
Cardiovascular complications in COVID-19 (2020, neutral): “Inhibition of ACE2 may be another factor in lung injury, as well as the cause of the systemic inflammation with cytokine release that can result in acute respiratory distress syndrome (ARDS) and multiorgan dysfunction [11] [12] [13] .”
Postmortem examination of COVID‐19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction (2020, result): “As ACE2 is up-regulated upon the administration of antihypertensive therapy affecting the RAAS, these agents might increase the susceptibility to viral invasion, thus increasing the risk of severe and lethal disease outcomes.(46) However, other experimental evidence has shown a protective effect of ”
The pivotal link between ACE2 deficiency and SARS-CoV-2 infection (2020, neutral): “[16,22,48] In other terms, the virus appears to entry into the cell along with the membrane receptor, which is functionally removed from the external site of the membrane.”
Insights into SARS-CoV-2 genome, structure, evolution, pathogenesis and therapies: Structural genomics approach (2020, neutral): “Whereas, SARS-CoV and SARS-CoV-2 recognize the ACE2 receptor to bind with the viral S protein [13].”
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): An overview of viral structure and host response (2020, positive): “This drug has been used clinically in the treatment of chronic pancreatitis so that it is considered to be a potential therapy for COVID-19 treatment [50] [51] [52] .”
COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up (2020, background): “binding the angiotensin converting enzyme 2 (ACE2) (12), which is highly expressed in lung alveolar cells, cardiac myocytes, the vascular endothelium, and other cells (1,13).”