Urotensin II: A Key Role in Hormonal and Inflammatory Cytokine Regulation in COVID-19 Patients

The COVID-19 pandemic exhibits a wide spectrum of severities and pathophysiological mechanisms. The virus targets angiotensin-converting enzyme 2 (ACE2) receptors, disrupting the renin-angiotensin-aldosterone system (RAAS) balance, which may explain various symptoms and risk factors. Fibrosis of the small airways is pivotal in the emergence of chronic obstructive pulmonary disease. Understanding these complex pathophysiological mechanisms is crucial for developing effective treatments and personalized approaches for COVID-19 patients. The present study is aimed at analyzing the concentrations of the clinical and laboratory parameters-such as hematological, biochemical, serological, angiotensin II (ANG II), endothelin-1 (ET-1), urotensin II (UII), and cortisol parameters-in patients with SARS-CoV-2 and evaluating the elevation of these parameters related to the pathogenicity. The study included two distinct groups: a healthy control group (n = 25) and a COVID-19 patient group (n = 75) during the period from August 2021 to January 2022. Cytokine levels were evaluated using commercially available enzyme-linked immunosorbent assay (ELISA) kits. The comparative analysis revealed that severe cases of COVID-19 have a significant elevation in the concentrations of hematological, biochemical, serological, and hormonal levels such as ANG II, ET-1, UII, and cortisol, as well as a substantial decline in the concentration of LYM%, in comparison with mild cases of COVID-19 and the control groups. Based on these findings, we concluded that ET-1, ANG II, and UII may be associated with COVID-19 pathophysiology and are linked to endothelial dysfunction, inflammation, and thrombosis.