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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium (Mg) fortification of drinking water succeeded in inhibition of atherogenesis development in a transgenic model of atherosclerosis-prone mice fed a high-cholesterol content diet. In order to delineate possible mechanisms of action of the anti-atherogenic effect of Mg, the involvement of LDL oxidation was studied. We determined the susceptibility of LDL to Cu+2 oxidation, anti-oxidized LDL antibody levels, and liver content of retinol and retinyl-palmitate. In order to study another possible mechanism we tested platelets interaction with extracellular matrix in both male and female mice with or without Mg fortification of drinking water. No difference was found in susceptibility of LDL to undergo oxidation. Female mice that received Mg had decreased anti-oxidized LDL antibody levels compared with control female mice, while there was no significant difference among male groups. On the other hand, only in the male group with Mg was a higher content of retinol and retinyl-palmitate found in the livers. Platelets coverage area on extracellular matrix was similar between groups. These results suggest that Mg might affect LDL oxidation, and thus atherogenesis.
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PMID:Mechanisms of action of the anti-atherogenic effect of magnesium: lessons from a mouse model. 1159 49

The precise correlation between magnesium and cardiovascular disease remains to be established. Matrix metalloproteinases (MMPs) are expressed in coronary arterial atherosclerotic lesions. MMP production in vascular smooth muscle cells (VSMCs) is stimulated by growth factors such as platelet-derived growth factor (PDGF). To assess the association between magnesium and MMPs, we examined the effects of different extracellular magnesium concentrations (0-3.0 mmol/l) on MMPs production in cultured rat VSMCs under basal and PDGF-stimulated conditions using gelatin zymography and western blotting. As magnesium is called a natural calcium antagonist, we further compared the effects of magnesium with some calcium antagonists. Magnesium reduced MMP-2 production dose-dependently at basal and PDGF-stimulated conditions in VSMCs. However, neither verapamil nor nifedipine influenced MMP-2 production under any conditions examined. The effect of magnesium on the production of MMP-2 was inhibited by two tyrosine kinase inhibitors-genistein and herbimycin A. The results of this study indicate that extracellularly added magnesium decreased MMPs secretion, which appears to be associated with protein tyrosine kinase.
Atherosclerosis 2003 Feb
PMID:Effects of magnesium on the production of extracellular matrix metalloproteinases in cultured rat vascular smooth muscle cells. 1253 39

Several data indicate that magnesium deficiency caused by poor diet and/or errors in its metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Experimentally induced low plasma levels of magnesium accelerate atherogenesis by increasing LDL concentrations and their oxidative modifications, and by promoting inflammation. In vitro studies have shown that low magnesium determines endothelial dysfunction, the initiating event leading to the formation of the plaque. Moreover, oral magnesium therapy has been shown to improve endothelial function in patients with coronary artery disease.Magnesium, which is an inexpensive, natural and rather safe element, could be useful in preventing atherosclerosis and as an adjuvant therapy in patients with clinical manifestations of the disease.
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PMID:Low magnesium and atherosclerosis: an evidence-based link. 1253 93

Magnesium (Mg) modulates blood lipid levels, atherogenesis, and atherosclerosis in rabbits, when supplemented to diet. We have recently reported that a high concentration (50 g/L) of Mg sulfate fortification of drinking water attenuates atherogenesis in male and female LDL-receptor-deficient mice fed a high-cholesterol diet. The aims of the current study were to examine whether lower concentrations and another Mg salt could also have such an antiatherogenic effect. Thirty male LDL-receptor-deficient mice were divided into three groups (n=10 in each group). The mice received either distilled water or water fortified with 0.83 g or with 8.3 g Mg-chloride per liter. In the first (27 wk) and second (5 wk) stages of the experiment, the mice received normal chow and Western-type diet, respectively. Blood was drawn for determination of plasma Mg, calcium, and lipid levels. The extent of atherosclerotic lesions was determined at the aortic sinus. Magnesium-chloride fortification of drinking water did not result in higher plasma Mg concentrations, whereas a trend toward lower plasma calcium concentrations did not reach statistical significance. Even though plasma lipid levels were similar at the beginning and the end of the study, there were decreased plasma cholesterol and triglyceride levels in the Mg groups after stage I. The atherosclerosis extent at the aortic sinus was significantly decreased in the 8.3-g Mg-chloride/L group (23,437 +/- 10,083 micron2) compared with the control group (65,937 +/- 31,761 microm2). There was also a trend toward lower atherosclerosis extent at the aortic sinus in the 0.83-g Mg-chloride/L group. An additional Mg salt (Mg-chloride) fortification of drinking water is capable of inhibiting atherogenesis in male LDL-receptor-deficient mice. That is done in a lower concentration of Mg than previously reported.
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PMID:Atherogenesis inhibition induced by magnesium-chloride fortification of drinking water. 1266 39

Magnesium supplementation has been reported to prevent cardiovascular diseases through the decrease of plasma lipids and to improve endothelial function in patients with coronary artery disease. In the present work, we evaluated whether high magnesium concentrations can directly affect the function of cultured endothelial cells, which play a crucial role in maintaining the functional integrity of the vascular wall. We cultured human umbilical vein endothelial cells for various times in media containing different concentration of magnesium (range 2 to 10 mM) and compared them to the corresponding controls (1 mM Mg). High Mg concentrations stimulated endothelial proliferation, enhanced the motogenic response to angiogenic factors and attenuated the response to lipopolysaccharide (LPS). In addition, we demonstrate that high concentrations of magnesium did not modulate the levels of plasminogen activator inhibitor-1, but enhanced the synthesis of nitric oxide, in part through the up-regulation of endothelial nitric oxide synthase. Our results demonstrate a direct role of magnesium in maintaining endothelial function. We therefore anticipate that magnesium may have a protective effect against atherosclerosis and could play a role in promoting the growth of collateral vessels in chronic ischemia. Moreover, because it induces the synthesis of nitric oxide, this cation could be a helpful tool in hypertension as well as in preventing thrombosis.
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PMID:High concentrations of magnesium modulate vascular endothelial cell behaviour in vitro. 1515 8

Low serum Mg2+ has been associated with an increased incidence of cardiovascular pathology in human populations. We investigated the effect of extracellular Mg2+ on Fe-catalyzed lipid peroxidation in rat aortic segments and in human aortic smooth muscle cells. Products of phospholipid oxidation [malonaldehyde (MDA) and 4-hydroxyalkenals (4-HA)], loss of fatty acyl double bonds (by proton-NMR) and glutathione levels indicated that exogenous ferric ions were several-fold more effective than ferrous ions in causing lipid peroxidation. Increased peroxidation was detectable at <1.0 microM Fe3+. Exogenous ferric iron-ionophore, 8-hydroxyquinoline, did not increase peroxidation by ferric ion, suggesting that Fe-catalyzed lipid peroxidation occurred at the cell surface. As ionized serum [Mg2+](o) was lowered from the physiological (0.7-0.96 mM) into the pathophysiological range (0.3-0.5mM) in Fe3+-containing medium, MDA/4-HA levels increased two to three-fold, with a concomitant loss of fatty acyl double bonds and decreased extracellular glutathione. Conversely, MDA/4-HA decreased as ionized Mg2+ was increased, accompanied by a rise in extracellular glutathione. The results indicate that Mg2+ protects aortic cell plasma membranes from ferric iron-catalyzed lipid peroxidation and that this is a contributing factor in the protective action of ionized Mg2+ on the cardiovascular system.
Atherosclerosis 2004 Jul
PMID:Iron-catalyzed lipid peroxidation in aortic cells in vitro: protective effect of extracellular magnesium. 1518 42

Magnesium plays essential roles in fundamental cellular reaction and physiological regulation of vascularture, nervous system, and organs. Accumulating findings have revealed that magnesium deficiency relates cardiovascular risk factors including elevated blood pressure, insulin resistance, dyslipidemia, platelet aggregation, and inflammatory reaction, and leads to atherosclerosis.
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PMID:[Magnesium, cardiovascular risk factors and atherosclerosis]. 1569 60

One of the factors involved in accelerated atherosclerosis in hemodialysis patients is dyslipidemia. In this study we considered factors involved in intensification of dyslipidemia in hemodialysis patients. This study was done on 36 maintenance hemodialysis patients. Serum lipoprotein (a), Triglyceride, Cholesterol, HDL-C,LDL-C and also serum Intact parathormone(iPTH), Calcium, Phosphorus, Magnesium were measured. In statistical analysis there was not any correlation between serum lipids and iPTH. There was not correlation between serum calcium with serum lipids (p > 0.05). There was not correlation between CaxP product with serum lipids (p > 0.05). There was a positive correlation between serum Magnesium and Lipoprotein(a) (P < 0.05) and also positive correlation between serum magnesium with triglyceride level (P < 0.05) was seen too. Magnesium doesn't increase the lipoprotein synthesis. It may involve in the regulation of some enzymes responsible for lipoprotein synthesis. Correlation of serum magnesium with serum triglycerides can be due to changes in hepatic triglyceride metabolism. Lipoprotein(a) is a non traditional factor of premature atherosclerosis, its association with serum magnesium needs more attention in hemodialysis patients.
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PMID:Correlation of serum magnesium with dyslipidemia in maintenance hemodialysis patients. 1584 6

According to the Vital Statistics Report published by the Japanese Ministry of Health and Welfare, heart disease and cerebrovascular disease are the main causes of death in Japan. The main pathological finding in these diseases is atherosclerosis and the main risk factors, besides the patient's age and diathesis, include hyperlipidemia, hypertension, diabetes, obesity and smoking. Among the aforementioned various risk factors, hyperlipidemia play a crucial role at the stage of atherosclerosis. The main pathological findings in atherosclerosis include abnormal reactions of neutrophils, lymphocytes and monocytes/macrophages, vascular smooth muscle cells and vascular endothelial cells, and the accumulation of cholesterol ester in the arterial wall. Previously, Mg(2+) deficit and the lower blood concentration of Mg(2+) was a frequent in patients with the main risk factors, hyperlipidemia, hypertension, diabetes, and obesity. Magnesium is necessary the activity of lecithin cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL), which lowers triglyceride levels and raises HDL-cholesterol levels. Moreover, Mg(2+)-ATP is also the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis, which associated with cholesterol levels. In this article, we first discuss the effect of Mg(2+) deficit on atherosclerosis, especially hyperlipidemia in bloodstream and liver. Then, based on recent studies including our own, we describe the Mg(2+) deficit and the relationships between risk factors for atherosclerosis, hypertension, oxidative stress, cholesterol reverse transport system, and the molecular mechanisms, especially peroxisome preoliferator-activated receptor (PPAR), which have the pleiotropic effect in atherosclerosis. The mechanism is likely the effect of Mg(2+) on atherosclerosis.
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PMID:[Lipid metabolism and magnesium]. 1627 15

Magnesium (Mg) plays an essential role in a wide range of fundamental cellular reactions in patients with ischemic heart disease. It has been well known that Mg plays a pivotal role in control of cardiac excitability, neuromuscular transmission, vasomotor tone, and blood pressure, among other functions. Especially, many epidemiological, experimental, and clinical studies support a pathological role for Mg in the etiology and development of major coronary risk factors as diabetes mellitus, hypertension, and hyperlipidemia as well as ischemic heart disease. Furthermore, the therapeutic value of Mg in the management of coronary risk factors and ischemic heart disease has been clarified. Dietary Mg supplementation should be considered as a preventive element in atherosclerosis and ischemic heart disease.
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PMID:Magnesium and ischemic heart disease: a review of epidemiological, experimental, and clinical evidences. 1654 43


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