tetano
Editor, Senior Moderator
Curr Hypertens Rep
. 2020 Aug 27;22(9):63.
doi: 10.1007/s11906-020-01078-6.
Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses
Eleni Gavriilaki[SUP] 1 [/SUP], Panagiota Anyfanti[SUP] 1 [/SUP], Maria Gavriilaki[SUP] 2 [/SUP], Antonios Lazaridis[SUP] 1 [/SUP], Stella Douma[SUP] 1 [/SUP], Eugenia Gkaliagkousi[SUP] 3 [/SUP]
Affiliations
Abstract
To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype RECENT FINDINGS: Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients.
Keywords: COVID-19; Complement; Endothelial dysfunction; SARS-COV-2; Thrombosis; Thrombotic microangiopathy.
. 2020 Aug 27;22(9):63.
doi: 10.1007/s11906-020-01078-6.
Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses
Eleni Gavriilaki[SUP] 1 [/SUP], Panagiota Anyfanti[SUP] 1 [/SUP], Maria Gavriilaki[SUP] 2 [/SUP], Antonios Lazaridis[SUP] 1 [/SUP], Stella Douma[SUP] 1 [/SUP], Eugenia Gkaliagkousi[SUP] 3 [/SUP]
Affiliations
- PMID: 32852642
- DOI: 10.1007/s11906-020-01078-6
Abstract
To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype RECENT FINDINGS: Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients.
Keywords: COVID-19; Complement; Endothelial dysfunction; SARS-COV-2; Thrombosis; Thrombotic microangiopathy.