COVID-19-Related Stroke.
Angiotensin-Converting Enzyme 2
Betacoronavirus
/ metabolism
COVID-19
Coronavirus Infections
/ blood
Disseminated Intravascular Coagulation
/ drug therapy
Female
Humans
Male
Pandemics
Peptidyl-Dipeptidase A
/ administration & dosage
Pneumonia, Viral
/ blood
Recombinant Proteins
/ administration & dosage
SARS-CoV-2
Stroke
/ drug therapy
Tissue Plasminogen Activator
/ blood
Angiotensin-converting enzyme 2 (ACE2)
COVID-19
Coagulopathy
SARS-CoV-2
Sepsis
Stroke
Journal
Translational stroke research
ISSN: 1868-601X
Titre abrégé: Transl Stroke Res
Pays: United States
ID NLM: 101517297
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
14
04
2020
accepted:
21
04
2020
revised:
14
04
2020
pubmed:
8
5
2020
medline:
23
5
2020
entrez:
8
5
2020
Statut:
ppublish
Résumé
The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a "sepsis-induced coagulopathy" and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the "harmful" ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy.
Identifiants
pubmed: 32378030
doi: 10.1007/s12975-020-00818-9
pii: 10.1007/s12975-020-00818-9
pmc: PMC7202903
doi:
Substances chimiques
Recombinant Proteins
0
Peptidyl-Dipeptidase A
EC 3.4.15.1
ACE2 protein, human
EC 3.4.17.23
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Tissue Plasminogen Activator
EC 3.4.21.68
Types de publication
Letter
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
322-325Subventions
Organisme : NINDS NIH HHS
ID : R01 NS112511
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS099455
Pays : United States
Organisme : NINDS NIH HHS
ID : UO1NS113356
Pays : United States
Organisme : NINDS NIH HHS
ID : R01NS112511
Pays : United States
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