| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T79 |
0-584 |
Sentence |
denotes |
In the setting of SARS-CoV-2 infection, the vascular endothelium appears to be targeted directly by the virus as well as the milieu of proinflammatory cytokines elicited by the immune response.48 ACE-2 is also expressed widely in extrapulmonary sites including blood vessels, heart, kidney, and intestine.49,50 Accordingly, viral RNA has been detected in urine and stool samples from patients with COVID-19.51,52 In this regard, it is currently hypothesized that viral entry via endothelial-expressed ACE-2 represents a mechanism by which the virus can enter and infect other tissues. |
| T80 |
585-685 |
Sentence |
denotes |
Recent experimental data have highlighted the ability of COVID-19 to infect human endothelial cells. |
| T81 |
686-1032 |
Sentence |
denotes |
Indeed, human blood vessel organoids, which closely resemble human capillaries, contain viral RNA after exposure to COVID-19 in vitro.53 Strikingly, the application of human recombinant soluble ACE-2 markedly inhibited viral infection in human capillary organoids, pointing to a direct role for endothelial ACE-2 in viral uptake in blood vessels. |
| T82 |
1033-1372 |
Sentence |
denotes |
Intriguingly, the uptake of SARS-CoV-2 into cells is associated with the downregulation of ACE-2 expression.54,55 This appears to play an important role in promoting a proinflammatory and prothrombotic milieu since ACE-2 plays a pivotal role in regulating the RAS (renin-angiotensin system), by degrading angiotensin II to angiotensin 1–7. |
| T83 |
1373-1619 |
Sentence |
denotes |
While angiotensin II induces vasoconstriction and promotes a proinflammatory/prothrombotic phenotype, angiotensin 1–7 opposes these effects via binding to the MAS receptor, which is widely expressed including on endothelial cells and platelets.55 |
