SARS-CoV-2 infection, discovered and isolated in Wuhan City, Hubei Province, China, causes acute atypical respiratory symptoms and has led to profound changes in our lives. COVID-19 is characterized by a wide range of complications, which include pulmonary embolism, thromboembolism and arterial clot formation, arrhythmias, cardiomyopathy, multiorgan failure, and more. The disease has caused a worldwide pandemic, and despite various measures such as social distancing, various preventive strategies, and therapeutic approaches, and the creation of vaccines, the novel coronavirus infection (COVID-19) still hides many mysteries for the scientific community. Oxidative stress has been suggested to play an essential role in the pathogenesis of COVID-19, and determining free radical levels in patients with coronavirus infection may provide an insight into disease severity. The generation of abnormal levels of oxidants under a COVID-19-induced cytokine storm causes the irreversible oxidation of a wide range of macromolecules and subsequent damage to cells, tissues, and organs. Clinical studies have shown that oxidative stress initiates endothelial damage, which increases the risk of complications in COVID-19 and post-COVID-19 or long-COVID-19 cases. This review describes the role of oxidative stress and free radicals in the mediation of COVID-19-induced mitochondrial and endothelial dysfunction.

Chronic venous disease (CVD) is among the most common diseases in industrialized countries and has a significant socioeconomic impact. The diversity of clinical symptoms and manifestations of CVD pose major challenges in routine diagnosis and treatment. Despite the high prevalence and the huge number of venous surgical interventions performed every day, a substantial proportion of the etiopathogenesis remains unclear. There are several widely advocated and generally valid theories of “peri-capillary fibrin cuffs” and “white cell trapping hypothesis”, which consider the role of venous reflux/obstruction, inflammation, vascular remodeling, hemodynamic changes, genetic and social risk factors. There are several specific provoking factors for the development of venous reflux: incompetence of the valve system, inflammation of the vascular wall, and venous hypertension. Over the past few years, increasing scientific data has demonstrated the link between oxidative stress, endothelial dysfunction, and vascular inflammation. High levels of oxidants and persistent inflammation can cause cumulative changes in hemodynamics, resulting in permanent and irreversible damage to the microcirculation and endothelial cells. Production of reactive oxygen species and expression of inflammatory cytokines and adhesion molecules are involved in a vicious cycle of venous wall remodeling. The interaction of ROS, and in particular, the superoxide anion radical, with nitric oxide leads to a decrease in NO bioavailability, followed by the initiation of prolonged vasoconstriction and hypoxia and impairment of vascular tone. This review addresses the role of ED, oxidative, and hemodynamic stress in the CVD mediation. Based on predefined inclusion and exclusion criteria, we conducted a systematic review of published scientific articles using PubMed, PMC Europe, Scopus, WoS, MEDLINE, and Google Scholar databases in the interval from 24 April 2002 to 1 April 2025. The current review included studies (n = 197) scientific articles, including new reviews, updates, and grey literature, which were evaluated according to eligibility criteria. The selection process was performed using a standardized form according to PRISMA rules, the manual search of the databases, and a double-check to ensure transparent and complete reporting of reviews. Studies had to report quantitative assessments of the relationship between vascular endothelial dysfunction, inflammation, oxidative stress, and shear stress in a chronic venous disease.