LDL as a Cause of Atherosclerosis

Tomkin, G. H.; Owens, D.

doi:10.2174/1876506801205010013

Cited by 51 publications

(33 citation statements)

References 86 publications

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“…Increase in cholesterol synthesis is facilitated by the enzyme HMGCoAreductase. Tomkin and Owens (12) state that the decrease in cholesterol synthesis resulting from inhibition of HMGCoA-reductase enzyme activity reduces LDL levels and vice versa. HMGCoA-reductase inhibitory activity is shown by statins used in the treatment of hypercholesterolemia.…”

Section: Discussionmentioning

confidence: 99%

“…(12,13) Uncontrolled hypercholesterolemia can develop into cardiovascular disease. Hypercholesterolemia is strongly associated with high total cholesterol and LDL levels in the blood.…”

Section: Discussionmentioning

confidence: 99%

“…The addition of substances that are structurally similar to the NPC1L1 may reduce the levels of cholesterol and LDL. (7,12,16) The second mechanism is inhibition of intestinal acyl-CoA cholesterol acyltransferase 2 (ACAT2). In mammals, ACAT2 is important for lipid esterification in enterocytes and the liver to produce cholesteryl ester which is useful for the formation of chylomicrons and VLDL.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, inhibition of HMG-CoA reductase may inhibit the cholesterol synthesis pathway so that the levels of cholesterol and LDL in the blood are reduced. (7,12,16) The fourth mechanism is activation of LDL receptors. Increasing the number and activity (upregulation) of LDL receptors may improve the cholesterol-LDL clearance from the circulation.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, cholesterol levels and LDL in the blood will decrease. (7,12,16) The sixth mechanism is activation of cytochrome P450 7A1 (CYP7A1) or cholesterol-7á-hydroxylase. Activation (up-regulation) of CYP7A1 is theoretically able to lower the cholesterol in the liver, causing blood cholesterol influx, and ultimately lowering cholesterol levels in the blood.…”

Section: Discussionmentioning

confidence: 99%

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Honey improves lipid profile of diet-induced hypercholesterolemic rats

Nurmasitoh

Pramaningtyas

2016

UnivMed

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BACKGROUNDCoronary heart disease (CHD) is a major cause of morbidity and mortality throughout the world, including Indonesia. One of the risk factors for CHD is hypercholesterolemia. One of the natural products that has been developed for the treatment of hypercholesterolemia is honey. Honey contains fructooligosaccharides, various vitamins, minerals, and enzymes which are supposedly able to lower blood cholesterol levels. This research aimed to study the influence of honey on the levels of blood total cholesterol, triglyceride, and low density lipoprotein (LDL) levels in Wistar rats. METHODSThis study was of experimental post test control group design. Twentyfour male Wistar rats (Rattus norvegicus) were randomly divided into 4 groups. K1 was the negative control group (with normal diet), K2 was the positive control group (with high-fat diet), P1 was fed a high-fat diet for 7 days, followed by high-fat diet plus honey for the next 7 days. P2 was fed a high-fat diet for 7 days, followed by regular diet plus honey for the next 7 days. After completion of this treatment, total cholesterol, triglycerides, and LDL levels were measured by the cholesterol oxidase phenol+aminophenazone (CHOD-PAP) method using enzymatic spectrophotometry principles. RESULTSThere were significant differences in total cholesterol, triglyceride, and LDL levels between all groups after day 15 (p<0.05). CONCLUSIONHoney supplementation was able to reduce the blood levels of total cholesterol, triglycerides, and LDL. Honey supplementation accompanied by non-cholesterol feeds could more effectively lower total cholesterol, triglycerides, and LDL serum levels in Wistar rats. Keywords

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Section: Discussionmentioning

confidence: 99%

“…(12,13) Uncontrolled hypercholesterolemia can develop into cardiovascular disease. Hypercholesterolemia is strongly associated with high total cholesterol and LDL levels in the blood.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Honey improves lipid profile of diet-induced hypercholesterolemic rats

Nurmasitoh

Pramaningtyas

2016

UnivMed

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Computational modeling of low‐density lipoprotein accumulation at the carotid artery bifurcation after stenting

Johari,

Menichini,

Hamady

et al. 2023

Numer Methods Biomed Eng

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Restenosis typically occurs in regions of low and oscillating wall shear stress, which also favor the accumulation of atherogenic macromolecules such as low‐density lipoprotein (LDL). This study aims to evaluate LDL transport and accumulation at the carotid artery bifurcation following carotid artery stenting (CAS) by means of computational simulation. The computational model consists of coupled blood flow and LDL transport, with the latter being modeled as a dilute substance dissolved in the blood and transported by the flow through a convection‐diffusion transport equation. The endothelial layer was assumed to be permeable to LDL, and the hydraulic conductivity of LDL was shear‐dependent. Anatomically realistic geometric models of the carotid bifurcation were built based on pre‐ and post‐stent computed tomography (CT) scans. The influence of stent design was investigated by virtually deploying two different types of stents (open‐ and closed‐cell stents) into the same carotid bifurcation model. Predicted LDL concentrations were compared between the post‐stent carotid models and the relatively normal contralateral model reconstructed from patient‐specific CT images. Our results show elevated LDL concentration in the distal section of the stent in all post‐stent models, where LDL concentration is 20 times higher than that in the contralateral carotid. Compared with the open‐cell stents, the closed‐cell stents have larger areas exposed to high LDL concentration, suggesting an increased risk of stent restenosis. This computational approach is readily applicable to multiple patient studies and, once fully validated against follow‐up data, it can help elucidate the role of stent strut design in the development of in‐stent restenosis after CAS.

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Role of free radical in atherosclerosis, diabetes and dyslipidaemia: larger‐than‐life

Singh

Devi

Gollen

2015

Diabetes Metabolism Res

142

107

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During the past few decades, there have been numerous studies related to free radical chemistry. Free radicals including reactive oxygen species (ROS) and reactive nitrogen species are generated by the human body by various endogenous systems, exposure to different physiochemical conditions, or pathological states, and have been implicated in the pathogenesis of many diseases. These free radicals are also the common by-products of many oxidative biochemical reactions in cells. When free radicals overwhelm the body's ability to regulate them, a condition known as oxidative stress ensues. They adversely alter lipids, proteins, and DNA, which trigger a number of human diseases. In a number of pathophysiological conditions, the delicate equilibrium between free radical production and antioxidant capability is distorted, leading to oxidative stress and increased tissue injury. ROS which are mainly produced by vascular cells are implicated as possible underlying pathogenic mechanisms in a progression of cardiovascular diseases including ischemic heart disease, atherosclerosis, cardiac arrhythmia, hypertension, and diabetes. This review summarizes the key roles played by free radicals in the pathogenesis of atherosclerosis, diabetes, and dyslipidaemia. Although not comprehensive, this review also provides a brief perspective on some of the current research being conducted in this area for a better understanding of the role free radicals play in the pathogenesis of atherosclerosis, diabetes, and dyslipidaemia.

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LDL as a Cause of Atherosclerosis

Cited by 51 publications

References 86 publications

Honey improves lipid profile of diet-induced hypercholesterolemic rats

Honey improves lipid profile of diet-induced hypercholesterolemic rats

Computational modeling of low‐density lipoprotein accumulation at the carotid artery bifurcation after stenting

Role of free radical in atherosclerosis, diabetes and dyslipidaemia: larger‐than‐life

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