The Characteristics and Roles of Advanced Oxidation Protein Products in Atherosclerosis

Abstract

Advanced oxidation protein products (AOPPs) are novel biomarkers of oxidative damage to proteins and a novel class of inflammatory mediators. AOPPs can promote oxidative stress (OS) and inflammation and thus participate in many pathophysiological disease processes. Atherosclerosis is a chronic inflammatory disease of blood vessels that is characterized by low-density lipoprotein infiltration into the endothelial intima and the formation of atherosclerotic plaques. Inflammation and OS are established risk factors for the formation of atherosclerosis. Accumulated studies show that AOPPs can accelerate the progression of atherosclerosis through OS and inflammation. Additionally, AOPPs can accelerate the formation of atherosclerotic plaques by inhibiting high-density lipoprotein receptor scavenger receptor class B type I-mediated high-density lipoprotein cholesterol reverse transport, leading to metabolic disturbances. Some studies have suggested that plasma AOPPs levels are independently positively correlated with blood pressure and are also independent risk factors for cardiovascular disease. AOPPs can trigger oxidative bursts of neutrophils, monocytes and phagocytic cells, increase the generation of reactive oxygen species and promote the secretion of cytokines to accelerate endothelial cell injury. Detecting the levels and inhibiting the formation of AOPPs may provide a novel approach to monitor the progress and improve the prognosis of atherosclerosis.

Oxidative Modifications in Advanced Atherosclerotic Plaques: A Focus on In Situ Protein Sulfhydryl Group Oxidation

“…Although several studies report that atherosclerotic plaques contain high concentrations of some amino acid oxidation products, caused mainly by carbonylation, ROS and RNS oxidation, or thiolation [8][9][10], limited information is available regarding the relationship between the accumulation of in situ oxidized proteins and atherosclerosis severity [11]. Furthermore, different oxidation-specific epitopes can be detected in blood and may reflect atherosclerosis manifestations [12]. At present, the mechanisms underlying the formation of these by-products and their relevance for disease progression are not completely understood and deserve further investigation.…”

<p>Ox-LDL Causes Endothelial Cell Injury Through ASK1/NLRP3-Mediated Inflammasome Activation via Endoplasmic Reticulum Stress</p>

“…1 The pathological features of ACVD are extremely complex, and include endothelial cell injury, lipid infiltration, and the secretion of inflammatory mediators; the sum of which eventually leads to the formation of large numbers of plaques on the walls of large and middle-sized arteries. 2,3 Lipid uptake, macrophage foam cell formation, and inflammatory responses are key events needed for the initiation of atherosclerosis. 4 Therefore, it is highly important to study biological mechanisms that might inhibit the formation of foam cells and reduce inflammatory reactions that lead to the development and progression of atherosclerosis.…”

Stanozolol promotes lipid deposition in the aorta through an imbalance in inflammatory cytokines and oxidative status in LDLr knockout mice fed a normal diet

“…These authors observed a decrease in the atheroma plaque after increase in the antioxidant activity on liver, which was followed by the increase in plasma antioxidant enzyme activity, indicating that oxidative stress on liver can affect atherosclerosis development. Recently, Ou et al described that the oxidative stress promoted by the increase in AOPP increased the production of inflammatory cytokines and free radicals, disordering lipoprotein metabolism and promoting the chemotaxis of monocytes and macrophages, all of which contribute to the formation of atherosclerosis.…”