2022
DOI: 10.1007/s10787-022-01015-w
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A closer look at endothelial injury-induced platelet hyperactivity and the use of aspirin in the treatment of COVID infection

Abstract: In this commentary, we make a case that the mechanism of COVID pathogenesis is related to virus-induced endothelial injury resulting in platelet activation and the formation of microthrombi both systemically and in cardiac and pulmnonary circulation which result in major causes of COVID morbidity and mortality. Aspirin by virtue of its irreversible inhibition of platelet COX-1, should reverse these platelet-induced pathogenic changes associated with COVID infection for the 6–9 day lifetime of the platelet. We … Show more

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Cited by 3 publications
(2 citation statements)
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References 15 publications
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“…SARS-CoV-2 contributes to platelet activation via various pathways, including directly binding to platelet surface, provoking endothelial injury, and sustaining the release of von Willebrand factor. 23 , 24 , 53 , 60 , 61 Firstly, SARS-CoV-2 directly binds to platelet angiotensin-converting enzyme 2 (ACE2), which can stimulate platelets, release coagulation factors and inflammatory cytokines, and promote the formation of platelet aggregates, 54 and Eric Boilard et al consider that platelet alpha and dense granule are elevated in blood are the source of inflammatory cytokines. 53 At the same time, Milka Koupenova et al consider through ACE2 or attached to microparticle by taking up virions, platelets can internalize the virus, resulting in platelet programmed death and release of platelet content; this response contributes to dysregulated functionality.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…SARS-CoV-2 contributes to platelet activation via various pathways, including directly binding to platelet surface, provoking endothelial injury, and sustaining the release of von Willebrand factor. 23 , 24 , 53 , 60 , 61 Firstly, SARS-CoV-2 directly binds to platelet angiotensin-converting enzyme 2 (ACE2), which can stimulate platelets, release coagulation factors and inflammatory cytokines, and promote the formation of platelet aggregates, 54 and Eric Boilard et al consider that platelet alpha and dense granule are elevated in blood are the source of inflammatory cytokines. 53 At the same time, Milka Koupenova et al consider through ACE2 or attached to microparticle by taking up virions, platelets can internalize the virus, resulting in platelet programmed death and release of platelet content; this response contributes to dysregulated functionality.…”
Section: Discussionmentioning
confidence: 99%
“…2 Platelet aggregation and macroplatelets in COVID-19 patients were also observed in peripheral blood smears, which indicated platelet hyperactivity. [23][24][25] However, there are few dynamic studies on whether platelet parameters change during the disease and recovery from COVID- 19.…”
Section: Introductionmentioning
confidence: 99%