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10.1016/j.ejphar.2020.173545

http://scihub22266oqcxt.onion/10.1016/j.ejphar.2020.173545
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suck abstract from ncbi


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pmid32926917      Eur+J+Pharmacol 2020 ; 887 (ä): 173545
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  • Should ACE2 be given a chance in COVID-19 therapeutics: A semi-systematic review of strategies enhancing ACE2 #MMPMID32926917
  • Kaur U; Acharya K; Mondal R; Singh A; Saso L; Chakrabarti S; Chakrabarti SS
  • Eur J Pharmacol 2020[Nov]; 887 (ä): 173545 PMID32926917show ga
  • 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.
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*drug therapy[MESH]
  • |Down-Regulation[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/*metabolism/*therapeutic use[MESH]
  • |Pneumonia, Viral/*drug therapy[MESH]


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