Introduction: SARS-CoV-2, the causative agent of COVID-19, has been shown to interact with angiotensin-converting enzyme 2 (ACE2) receptors expressed in various tissues, including endothelial cells. This interaction is associated with vascular injury, inflammation, and oxidative stress, which may contribute to multi-organ dysfunction in severe cases. To investigate the molecular basis of oxidative stress and endothelial activation in COVID-19, we analyzed the expression of selected biomarkers in tracheobronchial samples obtained from critically ill patients.
Methods: A case-control study was performed including 34 patients with COVID-19 admitted to the ICU (17 infected with the SARS-CoV-2 alpha variant and 17 with the omicron variant) confirmed by RT-qPCR, and 40 non-COVID-19 outpatients admitted to the bronchoscopy department as controls. Inclusion criteria included absence of diabetes and cardiovascular diseases and age between 30–80 years. Tracheobronchial secretions were collected, and the expression of ICAM-1, VCAM-1, NOX2, vWF, iNOS, and Nrf2 genes was evaluated using qRT-PCR with TaqMan and SYBR Green assays.
Results: COVID-19 patients showed significantly increased expression of ICAM-1, VCAM-1, NOX2, vWF, and iNOS, while Nrf2 expression was markedly reduced compared to controls. These findings highlight a combined process of endothelial activation, inflammation, and oxidative imbalance.
Conclusion: Our data suggest that COVID-19 induces a state of oxidative stress and endothelial activation, which may contribute to systemic inflammation and subsequent organ dysfunction. Molecular profiling of endothelial and oxidative stress markers may serve as a useful tool for understanding disease progression and identifying potential therapeutic targets in severe COVID-19.