The Role of Oxidative Stress in Atherosclerosis

Abstract

Atherosclerosis is a chronic inflammatory disease of the vascular system and is the leading cause of cardiovascular diseases worldwide. Excessive generation of reactive oxygen species (ROS) leads to a state of oxidative stress which is a major risk factor for the development and progression of atherosclerosis. ROS are important for maintaining vascular health through their potent signalling properties. However, ROS also activate pro-atherogenic processes such as inflammation, endothelial dysfunction and altered lipid metabolism. As such, considerable efforts have been made to identify and characterise sources of oxidative stress in blood vessels. Major enzymatic sources of vascular ROS include NADPH oxidases, xanthine oxidase, nitric oxide synthases and mitochondrial electron transport chains. The production of ROS is balanced by ROS-scavenging antioxidant systems which may become dysfunctional in disease, contributing to oxidative stress. Changes in the expression and function of ROS sources and antioxidants have been observed in human atherosclerosis while in vitro and in vivo animal models have provided mechanistic insight into their functions. There is considerable interest in utilising antioxidant molecules to balance vascular oxidative stress, yet clinical trials are yet to demonstrate any atheroprotective effects of these molecules. Here we will review the contribution of ROS and oxidative stress to atherosclerosis and will discuss potential strategies to ameliorate these aspects of the disease.

Blood Monocyte Phenotype Is A Marker of Cardiovascular Risk in Type 2 Diabetes

“…This accumulation of reactive oxygen species likely plays a prominent role in the development of atherosclerosis, as demonstrated by numerous studies. [52][53][54][55][56][57] Another phenomenon could have an impact, which is the release by activated monocytes of free mitochondria and microvesicles containing mitochondrial elements, as demonstrated by Puhm et al 58 The development of therapeutic interventions to limit this mitochondrial dysfunction and its impact on cardiovascular risk could be contemplated in patients with T2D, as is already the case in psychiatric 59 or neurological diseases. 60 Nevertheless, our study puts monocytes at the core of the equation for the heightened risk in patients with T2D and advocates for further research on antiatherosclerotic treatments targeting monocytes and mitochondrial dysfunction.…”

Extracellular vesicles and endothelial dysfunction in infectious diseases

“…ROS have been considered an important contributing factor to the development of endothelial dysfunction and a wide range of CVDs including HTN and atherosclerosis (Batty et al., 2022; Ferroni et al., 2006). H. pylori infection, especially CagA + H. pylori infection can increase ROS levels through various mechanisms, including increased productions of inflammatory cytokines and CagA‐containing exosomes mediated mechanism (Xia et al., 2022).…”

Enzyodynamic therapy at nanoscale

“…AS is a chronic inflammatory disease with the characteristic of increased intravascular ROS production. 151 Excessive ROS will cause the undesirable lipid peroxidation. The metabolite hydrogen peroxide produced in the process of lipid peroxidation can promote AS by directly damaging endothelial cells, increasing the adhesion and activity of neutrophils and enhancing the sensitivity of platelet aggregation.…”

“…AS is a chronic inflammatory disease with the characteristic of increased intravascular ROS production 151 . Excessive ROS will cause the undesirable lipid peroxidation.…”

“…Most importantly, it has been reported that CDs also have enzymatic activity. Luo et al 43 prepared a new type of CDs with red fluorescence that can be used as SOD nanozyme by heating the solution containing glutathione, folate and formamide, providing high potential for in vivo imaging and ALI treatment. Atherosclerosis (AS) AS is a chronic inflammatory disease with the characteristic of increased intravascular ROS production 151 . Excessive ROS will cause the undesirable lipid peroxidation.…”