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Updated: May 15, 2025
Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch
Published on: April 21, 2023
A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease-Inflammation, Oxidative Stress, and Shear
Hristo Abrashev1, Despina Abrasheva2, Nadelin Nikolov3
1Department of Vascular Surgery, Medical Faculty, Trakia University, 6000 Stara Zagora, Bulgaria.
Insights
Chronic venous disease (CVD) involves complex factors like endothelial dysfunction and oxidative stress. Understanding these mechanisms is key to improving diagnosis and treatment for this common condition.
Area of Science:
- Vascular Biology and Medicine
- Pathophysiology of Chronic Diseases
Background:
- Chronic venous disease (CVD) is highly prevalent, impacting socioeconomic factors, yet its etiopathogenesis remains incompletely understood.
- Existing theories like "peri-capillary fibrin cuffs" and "white cell trapping" highlight venous reflux, inflammation, and hemodynamic changes.
- Emerging evidence links endothelial dysfunction, oxidative stress, and vascular inflammation as critical contributors to CVD progression.
Purpose of the Study:
- To systematically review and synthesize current scientific data on the roles of endothelial dysfunction, oxidative stress, and hemodynamic stress in mediating chronic venous disease.
- To consolidate findings from a comprehensive literature search to clarify the interplay of these factors in CVD.
Main Methods:
- A systematic review of scientific articles published between April 2002 and April 2025.
- Literature search conducted across PubMed, PMC Europe, Scopus, WoS, MEDLINE, and Google Scholar databases.
- Inclusion of 197 studies reporting quantitative assessments of endothelial dysfunction, inflammation, oxidative stress, and shear stress in CVD, adhering to PRISMA guidelines.
Main Results:
- Oxidative stress and persistent inflammation lead to hemodynamic changes and irreversible microcirculatory damage.
- Reactive oxygen species (ROS) and inflammatory cytokines contribute to a cycle of venous wall remodeling.
- Impaired nitric oxide (NO) bioavailability due to ROS interaction results in vasoconstriction, hypoxia, and altered vascular tone.
Conclusions:
- Endothelial dysfunction, oxidative stress, and hemodynamic alterations are central to the pathophysiology of chronic venous disease.
- These factors create a detrimental cycle impacting vascular integrity and function.
- Further research clarifying these interactions is crucial for advancing CVD diagnosis and therapeutic strategies.
Abstract:
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.
