Oxidative Stress, Inflammation and Endothelial Dysfunction in COVID-19 Era and Long COVID-19 Complications

Dear Colleagues,

The imbalance between the production of reactive oxygen and nitrogen species (ROS and RNS), known as oxidative stress, plays a significant role in the pathogenesis of various diseases, including COVID-19. In the early stages of SARS-CoV-2 infection, ROS production helps to activate the immune response and inhibit viral replication. In SARS-CoV-2 infection, cytokine storm, which is an excessive immune response, leads to the overproduction of ROS and RNS, followed by a decrease in the antioxidant capacity of the body and the activation of redox-sensitive effector pathways. This disease progression includes a vicious circle of hyperinflammation, an overwhelming production of ROS, and oxidative stress, which leads to cell and tissue damage, followed by organ dysfunction, or COVID-19. The increased RONS levels cause the irreversible oxidation of important macromolecules such as lipids, proteins, carbohydrates, and DNA, and disrupt cellular homeostasis, which leads to apoptosis or necrosis.

The endothelium lines blood vessels and regulates vascular tone, blood flow, inflammation, and thrombosis. Oxidative stress-related endothelial damage with subsequent endothelial dysfunction plays a critical role in the pathophysiology of COVID-19, particularly in cases of severe COVID-19 and post-acute sequelae of COVID-19.

Abnormal levels of ROS lead to persistent endothelial cell proliferation and potentiate the development of long-term complications. Endothelial activation and an increased risk of thrombotic events are among the potentially life-threatening complications of COVID-19, and may lead to unpredictable outcomes. This Special Issue, entitled “Oxidative Stress, Inflammation and Endothelial Dysfunction in COVID-19 Era and Long COVID-19 Complications”, aims to collect manuscripts that present innovative molecular research associated with the role of ROS/RNS, ferroptosis, inflammation, mitochondrial dysfunction, endothelial damage, and macro- and microvascular thrombotic events in COVID-19 and long-COVID-19. We also welcome the submission of original articles, reviews, and clinical trials on the application of novel antioxidant strategies for the prevention and treatment of COVID-19.

Dr. Ekaterina Georgieva
Guest Editor

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• oxidative stress
• redox-disbalance
• COVID-19
• post-COVID-19
• cytokines
• mitochondrial dysfunction
• endothelial damages
• ROS and RNS
• thrombosis
• antioxidant therapy
• oxidative shock