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10.1007/s00408-020-00408-4

http://scihub22266oqcxt.onion/10.1007/s00408-020-00408-4
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33170317!7653219!33170317
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suck abstract from ncbi

pmid33170317      Lung 2020 ; 198 (6): 867-877
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  • ACE2: The Major Cell Entry Receptor for SARS-CoV-2 #MMPMID33170317
  • Scialo F; Daniele A; Amato F; Pastore L; Matera MG; Cazzola M; Castaldo G; Bianco A
  • Lung 2020[Dec]; 198 (6): 867-877 PMID33170317show ga
  • Despite the unprecedented effort of the scientific community, the novel SARS-CoV-2 virus has infected more than 46 million people worldwide, killing over one million two hundred thousand. Understanding the mechanisms by which some individuals are more susceptible to SARS-CoV-2 infection and why a subgroup of them are prone to experience severe pneumonia, and death should lead to a better approach and more effective treatments for COVID-19. Here, we focus our attention on ACE2, a primary receptor of SARS-CoV-2. We will discuss its biology, tissue expression, and post-translational regulation that determine its potential to be employed by SARS-CoV-2 for cell entry. Particular attention will be given to how the ACE2 soluble form can have a great impact on disease progression and thus be used in a potential therapeutic strategy. Furthermore, we will discuss repercussions that SARS-CoV-2/ACE2 binding has on the renin-angiotensin system and beyond. Indeed, although mostly neglected, ACE2 can also act on [des-Arg 937]-bradykinin of the kinin-kallikrein system regulating coagulation and inflammation. Thorough comprehension of the role that ACE2 plays in different pathways will be the key to assess the impact that SARS-CoV-2/ACE2 binding has on organismal physiology and will help us to find better therapies and diagnostic tools.
  • |Angiotensin-Converting Enzyme 2/*physiology[MESH]
  • |COVID-19/diagnosis/*etiology/therapy[MESH]
  • |Humans[MESH]
  • |Receptors, Coronavirus/physiology[MESH]
  • |Renin-Angiotensin System/physiology[MESH]
  • |SARS-CoV-2/*physiology[MESH]


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