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10.1161/HYPERTENSIONAHA.120.15353

http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.120.15353
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32476472!ä!32476472

suck abstract from ncbi

pmid32476472      Hypertension 2020 ; 76 (2): 294-299
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  • COVID-19: ACE2centric Infective Disease? #MMPMID32476472
  • Verdecchia P; Cavallini C; Spanevello A; Angeli F
  • Hypertension 2020[Aug]; 76 (2): 294-299 PMID32476472show ga
  • Diffuse pulmonary inflammation, endothelial inflammation, and enhanced thrombosis are cardinal features of coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2. These features are reminiscent of several adverse reactions triggered by angiotensin II and opposed by angiotensin(1-7), in many experimental models. Severe acute respiratory syndrome coronavirus 2 binds to ACE2 (angiotensin-converting enzyme 2) receptors and entries into the cell through the fusion of its membrane with that of the cell. Hence, it downregulates these receptors. The loss of ACE2 receptor activity from the external site of the membrane will lead to less angiotensin II inactivation and less generation of antiotensin(1-7). In various experimental models of lung injury, the imbalance between angiotensin II overactivity and of antiotensin(1-7) deficiency triggered inflammation, thrombosis, and other adverse reactions. In COVID-19, such imbalance could play an important role in influencing the clinical picture and outcome of the disease. According to this line of thinking, some therapeutic approaches including recombinant ACE2, exogenous angiotensin(1-7), and angiotensin receptor blockers seem particularly promising and are being actively tested.
  • |*Betacoronavirus[MESH]
  • |Angiotensin Receptor Antagonists/*therapeutic use[MESH]
  • |Angiotensin-Converting Enzyme Inhibitors/*therapeutic use[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*drug therapy/epidemiology/metabolism[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*drug therapy/epidemiology/metabolism[MESH]
  • |Renin-Angiotensin System/*drug effects[MESH]


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