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10.1038/s41598-020-76488-2

http://scihub22266oqcxt.onion/10.1038/s41598-020-76488-2
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33177594!7658217!33177594
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suck abstract from ncbi


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pmid33177594      Sci+Rep 2020 ; 10 (1): 19522
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  • SARS-CoV-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells #MMPMID33177594
  • Sidarta-Oliveira D; Jara CP; Ferruzzi AJ; Skaf MS; Velander WH; Araujo EP; Velloso LA
  • Sci Rep 2020[Nov]; 10 (1): 19522 PMID33177594show ga
  • SARS-CoV-2, the pathogenic agent of COVID-19, employs angiotensin converting enzyme-2 (ACE2) as its cell entry receptor. Clinical data reveal that in severe COVID-19, SARS-CoV-2 infects the lung, leading to a frequently lethal triad of respiratory insufficiency, acute cardiovascular failure, and coagulopathy. Physiologically, ACE2 plays a role in the regulation of three systems that could potentially be involved in the pathogenesis of severe COVID-19: the kinin-kallikrein system, resulting in acute lung inflammatory edema; the renin-angiotensin system, promoting cardiovascular instability; and the coagulation system, leading to thromboembolism. Here we assembled a healthy human lung cell atlas meta-analysis with ~ 130,000 public single-cell transcriptomes and show that key elements of the bradykinin, angiotensin and coagulation systems are co-expressed with ACE2 in alveolar cells and associated with their differentiation dynamics, which could explain how changes in ACE2 promoted by SARS-CoV-2 cell entry result in the development of the three most severe clinical components of COVID-19.
  • |*Blood Coagulation[MESH]
  • |*Gene Expression Profiling[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Betacoronavirus/enzymology/*genetics/physiology[MESH]
  • |Humans[MESH]
  • |Kallikrein-Kinin System/*genetics[MESH]
  • |Peptidyl-Dipeptidase A/*genetics[MESH]
  • |Pulmonary Alveoli/*cytology/metabolism[MESH]
  • |Renin-Angiotensin System/*genetics[MESH]
  • |SARS-CoV-2[MESH]


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