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10.1007/s11906-020-01078-6

http://scihub22266oqcxt.onion/10.1007/s11906-020-01078-6
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32852642!7449866!32852642
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suck abstract from ncbi


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pmid32852642      Curr+Hypertens+Rep 2020 ; 22 (9): 63
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  • Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses #MMPMID32852642
  • Gavriilaki E; Anyfanti P; Gavriilaki M; Lazaridis A; Douma S; Gkaliagkousi E
  • Curr Hypertens Rep 2020[Aug]; 22 (9): 63 PMID32852642show ga
  • To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype RECENT FINDINGS: Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients.
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*physiopathology[MESH]
  • |Endothelial Cells/pathology[MESH]
  • |Endothelium/*physiopathology/virology[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*physiopathology[MESH]


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