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COVID-19, Renin-Angiotensin System and Endothelial Dysfunction

Department of Pathology, School of Medicine, Boston University Medical Campus, Boston, MA 02118, USA
Authors to whom correspondence should be addressed.
Cells 2020, 9(7), 1652;
Received: 3 June 2020 / Revised: 4 July 2020 / Accepted: 7 July 2020 / Published: 9 July 2020
(This article belongs to the Special Issue COVID19, Renin-Angiotensin System and Endothelial Dysfunction)
The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak, which is caused by SARS-CoV-2 virus, has posed a serious threat to global public health and caused worldwide social and economic breakdown. Angiotensin-converting enzyme 2 (ACE2) is expressed in human vascular endothelium, respiratory epithelium, and other cell types, and is thought to be a primary mechanism of SARS-CoV-2 entry and infection. In physiological condition, ACE2 via its carboxypeptidase activity generates angiotensin fragments (Ang 1–9 and Ang 1–7), and plays an essential role in the renin-angiotensin system (RAS), which is a critical regulator of cardiovascular homeostasis. SARS-CoV-2 via its surface spike glycoprotein interacts with ACE2 and invades the host cells. Once inside the host cells, SARS-CoV-2 induces acute respiratory distress syndrome (ARDS), stimulates immune response (i.e., cytokine storm) and vascular damage. SARS-CoV-2 induced endothelial cell injury could exacerbate endothelial dysfunction, which is a hallmark of aging, hypertension, and obesity, leading to further complications. The pathophysiology of endothelial dysfunction and injury offers insights into COVID-19 associated mortality. Here we reviewed the molecular basis of SARS-CoV-2 infection, the roles of ACE2, RAS signaling, and a possible link between the pre-existing endothelial dysfunction and SARS-CoV-2 induced endothelial injury in COVID-19 associated mortality. We also surveyed the roles of cell adhesion molecules (CAMs), including CD209L/L-SIGN and CD209/DC-SIGN in SARS-CoV-2 infection and other related viruses. Understanding the molecular mechanisms of infection, the vascular damage caused by SARS-CoV-2 and pathways involved in the regulation of endothelial dysfunction could lead to new therapeutic strategies against COVID-19. View Full-Text
Keywords: SARS-CoV-2; endothelial dysfunction; ACE2; endothelial cell injury; CD209L; L-SIGN SARS-CoV-2; endothelial dysfunction; ACE2; endothelial cell injury; CD209L; L-SIGN
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MDPI and ACS Style

Amraei, R.; Rahimi, N. COVID-19, Renin-Angiotensin System and Endothelial Dysfunction. Cells 2020, 9, 1652.

AMA Style

Amraei R, Rahimi N. COVID-19, Renin-Angiotensin System and Endothelial Dysfunction. Cells. 2020; 9(7):1652.

Chicago/Turabian Style

Amraei, Razie, and Nader Rahimi. 2020. "COVID-19, Renin-Angiotensin System and Endothelial Dysfunction" Cells 9, no. 7: 1652.

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