Association between circulating oxidized low‐density lipoprotein and atherosclerotic cardiovascular disease

Abstract

Atherosclerosis is a chronic, progressive disease which eventually leads to coronary heart disease (CHD), ischemic stroke and other atherosclerotic cardiovascular disease (ASCVD). Numerous studies have demonstrated an atherogenic role of oxidized low-density lipoprotein (ox-LDL) in the progression of ASCVD. This article briefly reviews the atherogenic mechanism of ox-LDL, the methods of measuring ox-LDL in the circulation, effect of medical therapy and life-style modification on ox-LDL level, and the association between circulating ox-LDL and atherosclerosis, including clinical ASCVD events and subclinical atherosclerosis, in observational studies.

Human T lymphotropic virus type 1 and risk of cardiovascular disease: High‐density lipoprotein dysfunction versus serum HDL‐C concentrations

“…In states of systemic inflammation like atherosclerosis and chronic infections, lipoproteins can be modified and get oxidized. Although many studies described the relation of LDLox and atherosclerosis, the impact of LDLox on atherogenesis remains unclear [29]. Unlike LDL, HDL is part of the innate immunity and also has the ability to influence cholesterol availability in lipid rafts in immune cells resulting in the modulation of toll-like receptors, MHC-II complex, as well as B-and T-cell receptors, while specific molecules shuttled by HDL such as sphingosine-1-phosphate (S1P) contribute to immune cells trafficking.…”

Could Omega 3 Fatty Acids Preserve Muscle Health in Rheumatoid Arthritis?

“…DHA and EPA increased LDL particle size in hypertensive type 2 diabetes patients and with hypertriglyceridemia respectively, contributing to the protection against CVD [103,104]. Moreover, it was showed that omega 3 FA reduced circulating oxidized LDL and improved endothelial function in patients presenting a high risk for CVD [105][106][107]. Omega 3 FA directly replace proinflammatory omega 6 FA in biological membranes.…”

N‐acetylcysteine prevents oxidized low‐density lipoprotein‐induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells

“…The mechanisms for the poor survival of transplanted BMSCs have not been fully understood and are very likely multifactorial including inflammation, oxidative stress, mechanical stress and hypoxia. Oxidized low‐density lipoproteins (ox‐LDLs) are naturally present in serum and an important source for reactive oxygen species (ROS) and oxidative stress . Ox‐LDL has been shown to inhibit proliferation and endothelial differentiation of BMSCs, and induce apoptosis of BMSCs with both ROS‐dependent and ROS‐independent mechanisms .…”

“…Oxidized low-density lipoproteins (ox-LDLs) are naturally present in serum and an important source for reactive oxygen species (ROS) and oxidative stress. 8,9 Ox-LDL has been shown to inhibit proliferation and endothelial differentiation of BMSCs, and induce apoptosis of BMSCs with both ROS-dependent and ROS-independent mechanisms. 10,11 Our previous study showed that ox-LDL impaired the survival of BMSCs in vitro partially through direct cell membrane damage independent of ROS formation.…”