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|Title:||Endothelial dysfunction and covid-19 (Review)||Authors:||Daher, Jalil||Affiliations:||Department of Biology||Keywords:||Angiotensin converting enzyme 2
Angiotensin converting enzyme inhibitor
Angiotensin receptor blocker
Plasminogen activator inhibitor-1
Reactive oxygen species
|Issue Date:||2021||Part of:||Biomedical reports||Volume:||15||Issue:||6||Abstract:||
It is hypothesized that several comorbidities increase the severity of COVID-19 symptoms. Cardiovascular disease including hypertension was shown to play a critical role in the severity of COVID-19 infection by affecting the survival of patients with COVID-19. Hypertension and the renin-angiotensin-aldosterone system are involved in increasing vascular inflammation and endothelial dysfunction (ED), and both processes are instrumental in COVID-19. Angiotensin-converting enzyme 2 is an essential component of the renin-angiotensin-aldosterone system and the target receptor that mediates SARS-CoV-2 entry to the cell. This led to speculations that major renin-angiotensin-aldosterone system inhibitors, such as angiotensin receptor blockers and angiotensin-converting enzyme inhibitors might affect the course of the disease, since their administration enhances angiotensin-converting enzyme (ACE)2 expression. An increase in ACE2 activity could reduce angiotensin II concen-tration in the lungs and mitigate virus-driven lung injury. This could also be associated with a reduction in blood coagulation, which plays a critical role in the pathogenesis of SARS-CoV-2; of note, COVID-19 is now regarded as a disorder of blood clotting. Therefore, there is an urgent need to better understand the effect of targeting ACE2 as a potential treatment for SARS-CoV-2 driven injury, and in alleviating COVID-19 symptoms by reversing SARS-CoV-2-induced excessive coagulation and fatalities. Ongoing therapeutic strategies that include recombinant human ACE2 and anti-spike monoclonal antibodies are essential for future clinical practice in order to better understand the effect of targeting ED in COVID-19.
|URI:||https://scholarhub.balamand.edu.lb/handle/uob/5185||ISSN:||20499434||DOI:||10.3892/BR.2021.1478||Open URL:||Link to full text||Type:||Journal Article|
|Appears in Collections:||Department of Biology|
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