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10.1016/j.ijid.2020.05.002

http://scihub22266oqcxt.onion/10.1016/j.ijid.2020.05.002
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suck abstract from ncbi


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pmid32389847      Int+J+Infect+Dis 2020 ; 96 (ä): 348-351
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  • Urgent need for evaluating agonists of angiotensin-(1-7)/Mas receptor axis for treating patients with COVID-19 #MMPMID32389847
  • Shete A
  • Int J Infect Dis 2020[Jul]; 96 (ä): 348-351 PMID32389847show ga
  • ACE2 is a receptor of entry of SARS-CoV-2 into the host cells, and its upregulation has been implicated in increasing susceptibility of individuals to this infection. The clinical picture of COVID-19 suggests a role of ACE2 blockade, rather than its overexpression, in causing the pathogenesis. ACE2 blockade results in increased angiotensin II activity with simultaneous hampering of functions of angiotensin-(1-7)/MasR axis. Acute respiratory distress due to interstitial pulmonary fibrosis, cardiomyopathy and shock reported in COVID-19 patients can be explained by imbalanced angiotensin II and angiotensin-(1-7) activities. Failure of angiotensin II type 1 receptor blockers to control the severity of SARS-CoV-2 infections indicates the importance of simultaneous induction of angiotensin-(1-7)/MasR axis for correcting pathological conditions in COVID-19 through its anti-fibrotic, anti-inflammatory, vasodilatory, and cardioprotective roles. MasR agonists have also shown organ protective effects in a number of animal studies. Unfortunately, these agonists have not been tested in clinical studies. Their evaluation in seriously ill COVID-19 patients is urgently warranted to reduce mortality due to infection.
  • |*Betacoronavirus[MESH]
  • |Angiotensin II/physiology[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Animals[MESH]
  • |COVID-19[MESH]
  • |COVID-19 Drug Treatment[MESH]
  • |Coronavirus Infections/*drug therapy/etiology[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/physiology[MESH]
  • |Pneumonia, Viral/*drug therapy/etiology[MESH]
  • |Proto-Oncogene Mas[MESH]
  • |Proto-Oncogene Proteins/*agonists[MESH]
  • |Receptors, G-Protein-Coupled/*agonists[MESH]


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