Is the Reason of Increased D-Dimer Levels in COVID-19 Because of ACE-2-Induced Apoptosis in Endothelium?

Clin Appl Thromb Hemost. 2020 Jan-Dec:26:1076029620935526. doi: 10.1177/1076029620935526.
No abstract available

Publication types

  • Letter

MeSH terms

  • Alphacoronavirus / pathogenicity
  • Angiotensin II / pharmacology
  • Angiotensin-Converting Enzyme 2
  • Animals
  • Apoptosis* / drug effects
  • Betacoronavirus / pathogenicity*
  • Betacoronavirus / physiology
  • COVID-19
  • Caspase Inhibitors / pharmacology
  • Caspase Inhibitors / therapeutic use
  • Chikungunya virus / pathogenicity
  • Coronavirus Infections / blood
  • Coronavirus Infections / complications*
  • Coronavirus Infections / pathology
  • Coronavirus Infections / virology
  • Endothelium, Vascular / enzymology
  • Endothelium, Vascular / pathology
  • Endothelium, Vascular / virology*
  • Fibrin Fibrinogen Degradation Products / metabolism*
  • Host-Pathogen Interactions*
  • Humans
  • Models, Cardiovascular
  • Orthomyxoviridae / pathogenicity
  • Pandemics
  • Peptidyl-Dipeptidase A / physiology*
  • Pneumonia, Viral / blood
  • Pneumonia, Viral / complications*
  • Pneumonia, Viral / pathology
  • Pneumonia, Viral / virology
  • Receptors, Virus / physiology*
  • SARS-CoV-2
  • Swine
  • Thrombophilia / blood
  • Thrombophilia / etiology*
  • Virus Replication
  • Zika Virus / pathogenicity

Substances

  • Caspase Inhibitors
  • Fibrin Fibrinogen Degradation Products
  • Receptors, Virus
  • fibrin fragment D
  • Angiotensin II
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2

Supplementary concepts

  • Swine acute diarrhea syndrome coronavirus