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10.1007/s00277-020-04138-8

http://scihub22266oqcxt.onion/10.1007/s00277-020-04138-8
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suck abstract from ncbi


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pmid32583086      Ann+Hematol 2020 ; 99 (8): 1701-1707
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  • COVID-19-driven endothelial damage: complement, HIF-1, and ABL2 are potential pathways of damage and targets for cure #MMPMID32583086
  • Marchetti M
  • Ann Hematol 2020[Aug]; 99 (8): 1701-1707 PMID32583086show ga
  • COVID-19 pandemia is a major health emergency causing hundreds of deaths worldwide. The high reported morbidity has been related to hypoxia and inflammation leading to endothelial dysfunction and aberrant coagulation in small and large vessels. This review addresses some of the pathways leading to endothelial derangement, such as complement, HIF-1alpha, and ABL tyrosine kinases. This review also highlights potential targets for prevention and therapy of COVID-19-related organ damage and discusses the role of marketed drugs, such as eculizumab and imatinib, as suitable candidates for clinical trials.
  • |*Betacoronavirus[MESH]
  • |Antibodies, Monoclonal, Humanized/administration & dosage[MESH]
  • |COVID-19[MESH]
  • |Clinical Trials, Phase II as Topic/methods[MESH]
  • |Complement Inactivating Agents/*administration & dosage[MESH]
  • |Coronavirus Infections/drug therapy/*metabolism/pathology[MESH]
  • |Drug Delivery Systems/*methods[MESH]
  • |Endothelium, Vascular/drug effects/*metabolism/pathology[MESH]
  • |Humans[MESH]
  • |Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors/*metabolism[MESH]
  • |Imatinib Mesylate/administration & dosage[MESH]
  • |Pandemics/prevention & control[MESH]
  • |Pneumonia, Viral/drug therapy/*metabolism/pathology[MESH]
  • |Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism[MESH]
  • |SARS-CoV-2[MESH]


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