Endothelial dysfunction in patients with COVID-19 is a key mechanism for the development of complications

Abstract

SARS-CoV-2, a novel coronavirus infection that primarily affects the lungs, can induce multi-organ involvement. Arterial hypertension (AH), diabetes mellitus (DM), and obesity increase the risk of severe COVID-19, up to and including the development of a fatal cytokine storm. The risk of severe SARS-CoV-2 infection in persons with obesity and DM is associated with baseline systemic inflammation and immune system dysfunction. In addition, this category of patients is more likely to have post-COVID-19 syndrome and worsen the course of chronic diseases. Endothelial damage – direct (SARS-CoV-2 infection) and indirect (systemic inflammation) may play a crucial role in the development of COVID-19 complications. Angiotensin-converting enzyme 2 (ACE-2) expressed in human endothelium plays a fundamental role in the new coronavirus infection. SARS-CoV-2 uses it as a receptor to enter the cell, which leads to a decrease in the bioavailability of ACE-2 on the endotheliocytes surface. Once inside, the virus induces its apoptosis, leading to the development of a proinflammatory and procoagulant state and, as a result, vascular damage. Drugs including ACE inhibitors, ARB, beta-blockers, and statins are widely prescribed to patients with DM, AH, and CHD, the groups most at risk for COVID-19, and their effects on the endothelium are well known. New classes of hypoglycemic drugs, particularly glucagon-like peptide 1 (GLP-1) receptor agonists, have demonstrated the ability to affect systemic inflammation and improve prognosis in DM and CHD patients. In addition, they have a positive effect on BP and metabolic profile. The proven reduction in weight on the background of the use of GLP-1 may be an additional factor in determining the choice of this class of drugs. These effects can be used in COVID-19 patients with a high risk of severe course, as well as in persons with obesity in the post-COVID-19 condition.