A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease—Inflammation, Oxidative Stress, and Shear Stress

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3660 - 3660

Published: April 12, 2025

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

Language: Английский

The formation and function of calciprotein particles

Pflügers Archiv - European Journal of Physiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 23, 2025

Vertebrate extracellular fluids lie below the threshold for spontaneous calcium phosphate (Ca-Pi) precipitation; yet, they remain supersaturated enough to foster crystal growth if unchecked. Calciprotein particles (CPP) and their smaller precursor calciprotein monomers (CPM) have emerged as fast-acting "mineral buffers" that mitigate abrupt local oversaturation. Although these complexes typically contain only trace amounts of Ca-Pi relative total plasma levels, exhibit remarkably high turnover kinetics, with clearance from circulation within minutes, far outpacing hormonal loops operate on timescales hours days. By forming ephemeral colloidal assemblies, CPM/CPP help maintain fluid-phase stability avert uncontrolled crystallization "accidents" in microenvironments such intestine or bone-remodeling sites. However, under chronic mineral stress, kidney disease, multiple inhibitory factors (e.g., fetuin-A, pyrophosphate) can become deficient, enabling persistent generation more advanced, crystalline CPP species. These "modified" adsorb additional ligands apolipoproteins, microbial remnants, factors) been linked inflammatory pro-calcific changes vascular immune cells. Despite minor quantitative contribution, rapidly mobilized colloids may exert outsized influence skeletal homeostasis, underscoring need clarify origins, biological roles, potential therapeutic targeting disorders metabolism.

Language: Английский

Calciprotein particle-activated endothelial cells aggravate smooth muscle cell calcification via paracrine signalling

Cellular and Molecular Life Sciences, Journal Year: 2025, Volume and Issue: 82(1)

Published: April 26, 2025

Language: Английский