Scavenger Receptor BI Induced by HDL From Coronary Heart Disease May Be Related to Atherosclerosis

This study aims to determine whether dysfunctional High Density Lipoprotein (HDL) influenced the expression of scavenger receptor class B type Ⅰ (SR-B1) to determine reverse cholesterol transport. Blood samples obtained from coronary heart disease patients confirmed by angiography were collected. HDL was extracted from the blood via ultracentrifugation. Then, the HDL was injected into apoE−/− mice, and the HepG2 cells cultured with Dulbecco’s modified eagle medium (DMEM) were added the HDL extracted from coronary heart disease patients. As controls, normal cases without coronary heart disease (CHD) and patients with angina pectoris and acute myocardial infarction were used. The protein expression levels of SR-B1 were detected by western blot, and the lipid accumulation levels were detected by Oil Red O staining in both tissues and cell levels. These results revealed that the HDL obtained from CHD patients downregulate the SR-B1 expression in ex vitro and in vitro studies. In addition, dysfunctional HDL may result in lower SR-B1 expression levels. The degree of SR-B1 expression levels could be relative to the degree of coronary congestion. Along with the increase in severe coronary congestion, such as myocardial infarction, the SR-B1 expression levels were lower. The dysfunctional HDL derived from coronary heart disease patients decreased the expression of SR-B1, and promoted lipid accumulation.

High-Density Lipoprotein (HDL) Triglyceride and Oxidized HDL: New Lipid Biomarkers of Lipoprotein-Related Atherosclerotic Cardiovascular Disease

Lipid markers are well-established predictors of vascular disease. The most frequently measured lipid markers are total cholesterol, high-density lipoprotein (HDL)-cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglyceride. HDL reduces atherosclerosis by multiple mechanisms, leading to a reduced risk of cardiovascular disease, and HDL-C, as a metric of HDL quantity, is inversely associated with cardiovascular disease, independent of LDL-C. However, the quality of the HDL appears to be more important than its quantity, because HDL loses its antiatherogenic functions due to changes in its composition and becomes “dysfunctional HDL”. Although there is evidence of the existence of “dysfunctional HDL”, biomarkers for monitoring dysfunctional HDL in clinical practice have not yet been established. In this review, we propose a new lipid panel for the assessment of dysfunctional HDL and lipoprotein-related atherosclerotic cardiovascular disease. The lipid panel includes the measurement of lipid peroxide and triglyceride contents within HDL particles.

Dysfunctional HDL as a Therapeutic Target for Atherosclerosis Prevention

Hypercholesterolemia is one of the main risk factors for the development of atherosclerosis. Among the various lipoprotein classes, however, high density lipoproteins (HDL) are inversely associated with the incidence of atherosclerosis, since they are able to exert a series of atheroprotective functions. The central role of HDL within the reverse cholesterol transport, their antioxidant and anti-inflammatory properties and their ability to preserve endothelial homeostasis are likely responsible for HDL-mediated atheroprotection. However, drugs that effectively raise HDL-C failed to result in a decreased incidence of cardiovascular event, suggesting that plasma levels of HDL-C and HDL function are not always related. Several evidences are showing that different pathologic conditions, especially those associated with an inflammatory response, can cause dramatic alterations of HDL protein and lipid cargo resulting in HDL dysfunction. Established and investigational drugs designed to affect lipid metabolism and to increase HDL-C are only partly effective in correcting HDL dysfunction.