Endothelial dysfunction and COVID‑19 (Review)
Affiliations: Department of Biology, Faculty of Arts and Sciences, University of Balamand, Tripoli PO Box 100, Lebanon
- Published online on: October 7, 2021 https://doi.org/10.3892/br.2021.1478
Copyright: © Daher
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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 concentration 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.