| dc.creator | Gonçalves, Remy Martins | |
| dc.creator | Hottz, Eugenio D. | |
| dc.creator | Bozza, Patricia T. | |
| dc.date | 2023-06-10T16:24:29Z | |
| dc.date | 2023-06-10T16:24:29Z | |
| dc.date | 2023 | |
| dc.date.accessioned | 2023-09-26T21:57:53Z | |
| dc.date.available | 2023-09-26T21:57:53Z | |
| dc.identifier | GONÇALVES, Remy Martins; HOTTZ, Eugenio D.; BOZZ, Patricia T. Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences. Current Research in Immunology, v.4, 100058, Apr. 2023. | |
| dc.identifier | 2590-2555 | |
| dc.identifier | https://www.arca.fiocruz.br/handle/icict/58984 | |
| dc.identifier | 10.1016/j.crimmu.2023.100058 | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/8874197 | |
| dc.description | Concerns for the long-term effects of COVID-19 infection have grown due to frequently reported persisting
symptoms that can affect multiple systems for longer than 4 weeks after initial infection, a condition known as
long-COVID-19 or post-acute COVID-19 syndrome (PACS). Even nonhospitalized survivors have an elevated risk
for the development of thromboinflammatory-associated events, such as ischemic stroke and heart failure,
pulmonary embolism and deep vein thrombosis. Recent findings point to the persistence of many mechanisms of
hypercoagulability identified to be associated with disease severity and mortality in the acute phase of the
disease, such as sustained inflammation and endotheliopathy, accompanied by abnormal fibrin generation and
impaired fibrinolysis. Platelets seem to be central to the sustained hypercoagulable state, displaying hyperreactivity
to stimuli and increased adhesive capacity. Platelets also contribute to elevated levels of thromboinflammatory
mediators and pro-coagulant extracellular vesicles in individuals with ongoing PACS. Despite new
advances in the understanding of mechanisms sustaining thromboinflammation in PACS, little is known about
what triggers this persistence. In this graphical review, we provide a schematic representation of the known
mechanisms and consequences of persisting thromboinflammation in COVID-19 survivors and summarize the
hypothesized triggers maintaining this prothrombotic state. | |
| dc.format | application/pdf | |
| dc.language | eng | |
| dc.publisher | Elsevier B.V. | |
| dc.rights | open access | |
| dc.subject | Síndrome pós-aguda de COVID-19 (PACS) | |
| dc.subject | Ativação plaquetária | |
| dc.subject | Hipercoagulabilidade | |
| dc.subject | Tromboinflamação | |
| dc.subject | Post-acute COVID-19 syndrome (PACS) | |
| dc.subject | Platelet activation | |
| dc.subject | Hypercoagulability | |
| dc.subject | Thromboinflammation | |
| dc.title | Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences | |
| dc.type | Article | |
