Inhibiting Low-Density Lipoproteins Intimal Deposition and Preserving Nitric Oxide Function in the Vascular System
Christophe Wiart in Medicinal Plants in Asia for Metabolic Syndrome, 2017
Vascular endothelial cells release nitric oxide which relaxes and suppresses abnormal proliferation vascular smooth muscle cells and inhibit low-density lipoprotein oxidation involved in atherogenesis. Thus, inhibiting low-density lipoproteins intimal deposition and oxidation and preserving nitric oxide function in arteries constitutes one therapeutic strategy to prevent cardiovascular pathologies associated with diabetes and obesity. The progressive deposition of cholesteryl ester and fibrous elements in arterial intima leads to atherosclerosis. Hypertension is one of the greatest public health problems, and it is estimated that by 2025 about 60% of the world population will suffer from it. Atherogenesis encompasses the entry and chronic deposition of low-density lipoprotein in arterial intima. The antithrombotic and antiatherogenic properties of nitric oxide produced by endothelial cells are due to the ability of this signaling molecule to inhibit low-density lipoprotein oxidation, intimal vascular smooth muscle cells migration, and proliferation.
Lipoproteins and their metabolism
Paul Durrington in Hyperlipidaemia 3Ed, 2007
The lipoproteins are macromolecular complexes of lipids and protein (Figure 2.1). Great diversity of composition and physical properties are possible, particularly in disease but also in health. As such, their classification and definition is particularly difficult. Each lipoprotein has a wide range of components, each with its own metabolic origin and fate. The components of lipoprotein undergo a complex metabolic interplay with receptors and with enzymes located on the lipoproteins, and on the capillary endothelium and between the circulating lipoproteins themselves, both in the vascular compartment and within the tissue fluid space. It is thus naive in the extreme to try to think of serum cholesterol or triglycerides in the same way as serum sodium or glucose, which are transported simply as solutes. The very existence of lipids within the circulation is dependent on lipoproteins.
Lipoprotein Metabolism and Implications for Atherosclerosis Risk Determination and Treatment Decisions
P. K. Shah in Risk Factors in Coronary Artery Disease, 2006
Investigators have extended the work of Dr. John Gofman and colleagues to involve a plethora of investigations that assessed the role of lipoprotein subclasses within the entire subclass distribution and their relationship to atherosclerosis. Lipoproteins are a diverse group of spherical particles that can be separated into various categories based on their density. Lipoprotein lipase (LDL) is a lipolytic enzyme located on the surface of vascular endothelial cells and on macrophages. It is responsible for TG hydrolysis and is the rate-limiting step for the uptake of lipoprotein TG and resultant fatty acids into adipose tissue and muscle. Phospholipid transfer protein mediates transfer of phospholipids from triglyceride-rich lipoproteins to high-density lipoprotein. The combination of elevated triglycerides and elevated LDL-C is termed combined hyperlipidemia, and when a family history of hyperlipidemia or atherosclerosis is present, it is termed familial combined hyperlipidemia.
Cradle-to-grave atherosclerosis: high density lipoprotein cholesterol.
Published in Journal of the American College of Nutrition, 1982
This presentation reviews environmental and genetic factors that relate to high density lipoprotein cholesterol, the most potent independent lipoprotein risk factor for coronary heart disease. Although at least three decades of work have focused upon the primary atherogenic lipoprotein, low density lipoprotein cholesterol (C-LDL), which has a strong positive association with coronary heart disease (CHD), it has only been in the past decade that detailed epidemiologic and biochemical studies have revealed that high density lipoprotein cholesterol (C-HDL) is the most potent lipoprotein cholesterol related to coronary heart disease; this relationship is, however, inverse.
Serum Beta-Lipoprotein Subfractions in Polyacrylamide Gel Electrophoresis Associated with Coronary Heart Disease
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 1976
L. Ose, T. Kalager, Inger K. Grundt
Subfractions of β-lipoprotein occurred more frequently in serum from patients with coronary heart disease than in serum from patients with no sign of coronary heart disease. Two β-lipoprotein subfractions were observed in polyacrylamide gel electrophoresis. The sera containing a β-lipoprotein sub-fraction with a position close to the β-lipoprotein band showed Lp(a) antigenic properties. Triglycerides were raised in the sera with β-lipoprotein subfractions. The cholesterol level was significantly higher in the coronary heart disease group but was not correlated to the presence of the β-lipoprotein subfraction. The β-lipoprotein subfraction may possibly represent an additional risk factor in the genesis of coronary heart disease, even in the absence of other hyperlipoproteinemias.
Association of lipoprotein(a) with platelet aggregation and thrombogenicity in patients undergoing percutaneous coronary intervention
Published in Platelets, 2021
Pei Zhu, Xiao-Fang Tang, Ying Song, Yin Zhang, Li-Jian Gao, Zhan Gao, Jue Chen, Yue-Jin Yang, Run-Lin Gao, Bo Xu, Jin-Qing Yuan
This study aimed to evaluate the association of lipoprotein(a) levels with platelet aggregation and thrombogenicity in patients undergoing percutaneous coronary intervention (PCI), and to investigate the ischemic outcome on this population. Lipoprotein(a) and modified thrombelastography were measured in 6601 consecutive patients underwent PCI on dual antiplatelet therapy. Cox proportional regression analysis was applied to illustrate the ischemic events in a 2-year follow up. The mean levels of lipoprotein(a) were 29.0 mg/dl. Patients with higher lipoprotein(a) levels had significantly accelerated fibrin generation (lower K time and bigger α angle) and greater clot strength (higher maximum amplitude (MA)) than patients with lower lipoprotein(a) levels (P < .001). Moreover, the higher lipoprotein(a) group also exhibited significantly higher adenosine diphosphate (ADP) induced platelet aggregation (MAADP) by thrombelastography platelet mapping assay than lower lipoprotein(a) group. Cox regression analyzes revealed that patients with higher lipoprotein(a) levels had a 16% higher risk of major adverse cardiovascular and cerebrovascular events (HR 1.159, 95%CI: 1.005–1.337, P = .042) compared with patients with lower lipoprotein(a) levels. This association persisted after adjustment for a broad spectrum of risk factors (HR 1.174, 95%CI: 1.017–1.355, P = .028). High plasma lipoprotein(a) levels were associated with increased platelet aggregation and ischemic events in patients underwent PCI. Lipoprotein(a) might indicate the need for prolonged antiplatelet therapy.