ACE2: A Double-Edged Sword Against SARS CoV-2 Associated Cardiovascular Complications and Endothelial Dysfunction

The outbreak of novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) during late December 2019 in Wuhan, Hubei Province, China, has become a pandemic of global concern in a very short time, impacting human life and economic slowdown. The severity of SARS-CoV2 infection can be ascertained by an increased number of human deaths, specifically in older populations and patients with predisposed cardiovascular disease (CVD) complications. SARS CoV-2 binds to Angiotensin-Converting Enzyme-2 (ACE2) receptors on host cells, followed by its internalization, rapid multiplication, and instigate cytokine storm. This review aims to decipher the role of ACE2 in SARS-CoV2 infected patients with pre-existing CVD conditions. While in CVD patients, stimulation of ACE2 expression protects against CVD-associated complications through antagonizing the detrimental effects of Angiotensin II (Ang II) to maintain vascular homeostasis and production of nitric oxides in blood vessels. It is still unclear why CVD patients are at higher risk of SARS-CoV2 infection and have a higher mortality rate. Endothelial Cells (ECs) are monolayers of cells covering the inner wall of blood vessels and all major organs in our body. They play an essential role in maintaining normal vasculature; therefore, ECs dysfunction has been considered the CVD hallmark. Improvement in CVD is related to the restoration of ECs function. Exploring the role of ECs dysfunction concerning the SARS-CoV2-CVD molecular axis could help decipher why CVD patients are at increased risk of novel coronavirus-related fatalities.