Abstract:
The severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) has resulted in almost 28 million cases of COVID-19 (Corona virus disease-2019) and more than 900000 deaths worldwide since December 2019. In the absence of effective antiviral therapy and vaccine, treatment of COVID-19 is largely symptomatic. By making use of its spike (S) protein, the virus binds to its primary human cell receptor, angiotensin converting enzyme 2 (ACE2) which is present in the pulmonary epithelial cells as well as other organs. SARS-CoV-2 may cause a downregulation of ACE2. ACE2 plays a protective role in the pulmonary system through its Mas-receptor and alamandine-MrgD-TGR7 pathways. Loss of this protective effect could be a major component of COVID-19 pathogenesis. An attractive strategy in SARS-CoV-2 therapeutics would be to augment ACE2 either directly by supplementation or indirectly through drugs which increase its levels or stimulate its downstream players. In this semi-systematic review, we have analysed the pathophysiological interplay between ACE and ACE2 in the cardiopulmonary system, the modulation of these two proteins by SARS-CoV-2, and potential therapeutic avenues targeting ACE-Ang II and ACE2-Ang (1–7) axes, that can be utilized against COVID-19 disease progression.
【저자키워드】 COVID-19, diabetes, Angiotensin converting enzyme-2, RAAS, Angiotensin II, Ang (1–7), 【초록키워드】 Treatment, SARS-CoV-2, antiviral therapy, Corona virus, ACE2, Vaccine, Cardiopulmonary, drug, progression, virus, COVID-19 disease, Protein, COVID-19 pathogenesis, symptomatic, therapeutic, death, receptor, protective effect, ACE, Pathways, pulmonary epithelial cell, acute respiratory syndrome, modulation, enzyme, other organs, protective role, downregulation, downstream, human cell, Loss, effective, bind, analysed, absence, stimulate, pathophysiological, pulmonary system, 【제목키워드】 ACE2,