Involvement of Spike Protein, Furin, and ACE2 in SARS-CoV-2-Related Cardiovascular Complications

Abstract

The novel coronavirus disease 2019 (COVID-19) is a global epidemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). SARS-CoV-2 has a similar structure to severe acute respiratory syndrome coronavirus-1(SARS-CoV-1). The S protein on the surface of the virus is cleaved by host proprotein convertases (PCs) to expose the active N-terminal S1 extracellular domain. Its receptors are angiotensin-converting enzyme 2 (ACE2), and the C-terminal S2 membrane anchoring protein is responsible for translocating the virus into the cell. Among patients with COVID-19, there is a higher prevalence of cardiovascular disease, and more than 7% of patients have suffered myocardial damage due to the infection, but the internal mechanism is still poorly understood. There is currently no specific and effective targeted treatment. Reduction of the patient’s morbidity and mortality is an urgent problem that needs to be solved clinically. By exploring the theoretical analysis of PCs and ACE2 in COVID-19 cardiovascular susceptibility, some insights on how to prevent and alleviate adverse cardiovascular prognosis have been provided in this study.