What cellular mechanisms are related to thromboembolic events in patients with COVID-19?
Cristian Rodrigues do NascimentoJúlio Martinez Martinez SantosSávio Breno Pires BritoPedro Pereira TenórioPublished in: Jornal vascular brasileiro (2021)
SARS-CoV-2 is the virus responsible for the COVID-19 pandemic. This disease is beginning to be better understood in terms of its other, non-respiratory, clinical manifestations. Over the course of months caring for patients infected by the virus, clinical and laboratory changes have been identified that have prompted researchers to debate the potential that SARS-CoV-2 has to trigger an exacerbated immune response that is capable of changing endothelial homeostasis through both direct and indirect mechanisms. With the intention of contributing to this debate, a review was conducted of the possible mechanisms that could trigger these phenomena in patients with COVID-19. It is important to understand the pathophysiology of the immunological mechanisms related to this disease in order to understand the potential endothelial damage that COVID-19 can provoke.
Keyphrases
- sars cov
- immune response
- respiratory syndrome coronavirus
- end stage renal disease
- coronavirus disease
- ejection fraction
- endothelial cells
- newly diagnosed
- chronic kidney disease
- oxidative stress
- prognostic factors
- atrial fibrillation
- toll like receptor
- risk assessment
- inflammatory response
- patient reported outcomes
- climate change
- respiratory tract