Title:Xanthine Oxidoreductase in the Pathogenesis of Endothelial Dysfunction:
An Update
Volume: 20
Issue: 1
Author(s): Rajat Mudgal and Sanjiv Singh*
Affiliation:
- Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research,
Hajipur, Bihar, India
Keywords:
Endothelial dysfunctions, xanthine oxidoreductase, vascular physiology, inflammation, ROS, vascular cells.
Abstract: Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in the formation of uric acid (UA) and is
involved in the generation of reactive oxygen species (ROS). Overproduction of ROS has been linked to the
pathogenesis of hypertension, atherosclerosis, and cardiovascular disease, with multiple studies over the last
30 years demonstrating that XOR inhibition is beneficial. The involvement of XOR and its constituents in the
advancement of chronic inflammation and ROS, which are responsible for endothelial dysfunction, is the focus
of this evidence-based review. An overabundance of XOR products and ROS appears to drive the inflammatory
response, resulting in significant endothelium damage. It has also been demonstrated that XOR activity
and ED are connected. Diabetes, hypertension, and cardiovascular disease are all associated with endothelial
dysfunction. ROS mainly modifies the activity of vascular cells and can be important in normal vascular physiology
as well as the development of vascular disease. Suppressing XOR activity appears to decrease endothelial
dysfunction, probably because it lessens the generation of reactive oxygen species and the oxidative stress
brought on by XOR. Although there has long been a link between higher vascular XOR activity and worse clinical
outcomes, new research suggests a different picture in which positive results are mediated by XOR enzymatic
activity. Here in this study, we aimed to review the association between XOR and vascular endothelial
dysfunction. The prevention and treatment approaches against vascular endothelial dysfunction in atherosclerotic
disease.
