Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium--aluminum (Mg--Al) alloy wire was surgically implanted in the abdominal aorta and carotid and renal arteries of virgin (no arterial disease) and breeder (testicular and ovarian arterial lesions) spontaneously hypertensive rats (SHR). The Mg--Al implants promptly dissolved causing increased adrenal glandular weight, thymic involution, depression of the abnormally elevated blood pressure, and poor growth. Serum enzymes (CPK, SGOT, SGPT and LDH) were elevated, circulating levels of triglycerides and cholesterol were reduced, corticosterone and deoxycorticosterone secretion increased. Histologically, fibrocellular, intimal lesions, rich in ground substance, developed about the Mg-Al implants. Occlusive thromboses with cholesterol-positive clefts appeared in the Mg-Al-implanted carotid arteries of breeder SHR with preexisting arterial (limited to gonadal arterioles) disease. It is suggested that adrenocortical and gonadal hormonal factors may condition the responsiveness of the arterial wall of SHR to injury and repair.
Atherosclerosis 1980 Aug
PMID:Pathophysiologic responses of spontaneously hypertensive rats to arterial magnesium--aluminum wire implants. 741 74

The properties and characteristics of acyl-CoA synthetase from the arterial wall of rats were investigated. The enzyme is located mainly in the microsomes. Its activity was found to be maximal at pH 7.0-8.0, and to be completely dependent on ATP, CoASH and Mg2+. The Km values for these substances were the same as those of the enzyme in liver. The activity was affected by serum, divalent cations, albumin, lipoproteins and phospholipids. In rats, the activity was decreased in various pathological conditions, such as tocopherol deficiency, hypertension and diabetes mellitus and was increased in hypercholesterolemia. The physiological significance of this enzyme in free fatty acid metabolism is discussed on the basis of these results.
Atherosclerosis 1980 Nov
PMID:Studies on acyl-CoA synthetase in rat arterial wall. 745 88

An important characteristic of hyperlipaemia associated with magnesium deficiency in rats is the postprandial accumulation of triglyceride-rich lipoproteins (TGRLP). The present investigation was performed to determine the susceptibility of TGRLP isolated from magnesium-deficient rats to metal ion and cell dependent peroxidation and the effect of these lipoproteins on cultured vascular smooth muscle cells (VSMC). TGRLP were isolated by sequential ultracentrifugation from plasma of control and magnesium-deficient rats fed for 8 d on adequate or magnesium-deficient diets. Magnesium-deficient animals were hypertriglyceridemic as compared to control rats. After exposure to oxidative stress in vitro, Cu2+ or activated macrophages, conjugated diene production was significantly higher in TGRLP isolated from magnesium-deficient rats. Culture of VSMC with TGRLP from magnesium-deficient rats resulted in more important cell growth than with lipoproteins isolated from control animals. After incubation with VSMC, TGRLP from magnesium-deficient rats showed higher conjugated diene production than those from control rats. These results support the atherogenic properties of magnesium deficiency, which is accompanied by hyperlipaemia and which affects two important linked pathways in atherosclerosis, lipoprotein peroxidation and VSMC proliferation.
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PMID:Triglyceride-rich lipoproteins from magnesium-deficient rats are more susceptible to oxidation by cells and promote proliferation of cultured vascular smooth muscle cells. 754 76

Magnesium (Mg) is the second most abundant intracellular cation and is a cofactor in more than 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Ionized Mg is the physiologically active form of the element. Protein-bound and chelated Mg buffer the ionized pool. Approximately half the total Mg in the body is present intracellularly in soft tissue, and the other half is present in bone. Less than 1% of the total body Mg is present in blood. However, the majority of our clinical laboratory information comes from the determination of total Mg in serum. Currently, the clinical laboratory evaluation of Mg status is limited primarily to the total serum Mg concentration and a 24-hour urinary excretion. Instrumentation to determine ionized Mg in serum (ion-selective electrode) and in soft tissue (nuclear magnetic resonance spectroscopy) should be available in the near future. Magnesium may be a factor in the treatment of acute myocardial infarction and the rate of atherosclerosis. Chronic changes of Mg status, that may be latent, are poorly understood and require a better knowledge of ionized Mg metabolism.
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PMID:Magnesium: the fifth but forgotten electrolyte. 794 27

Vascular smooth muscle cells (SMCs) in the media of normal arteries express alpha 1 beta 1 integrin with no detectable alpha 2 beta 1 as determined by immunocytochemistry. In contrast, immunoprecipitation of integrins expressed by human SMCs cultured from medial explants shows strong expression of alpha 2 beta 1 and no expression of alpha 1 beta 1. The apparent reciprocal expression of these two collagen and laminin receptors was confirmed by flow cytometric analysis of fluorescent labeled cells. Freshly isolated SMCs had detectable alpha 1, alpha 3, alpha 5, and alpha v subunits with low levels of detectable beta 3 and no detectable alpha 2. Cultured SMCs expressed alpha 2, alpha 3, alpha 5 and alpha v subunits with little or no alpha 1 or beta 3. Neither alpha 4 nor alpha 6 were detectable in freshly isolated or cultured cells. Expression of alpha 2 beta 1 receptors by cultured SMCs appears to be required for the migration of these cells on type I collagen. Migration of cultured SMCs across a type I collagen-coated membrane toward two different chemotactic stimuli, platelet-derived growth factor-BB (1 nmol/L) and insulin-like growth factor-(1 nmol/L), was Mg2+ dependent and inhibited by preincubation of cells with an affinity-purified polyclonal anti-alpha 2 beta 1 antibody or by monoclonal antibodies directed against the individual alpha 2 or beta 1 subunits. Attachment to type 1 collagen membranes was not affected by antibodies under conditions where migration was significantly impeded. The combined data show that SMC expression of alpha 1 beta 1 and alpha 2 beta 1 integrin receptors for collagen and laminin is dynamic and reciprocal and may be important with respect to SMC migration on type I collagen. These findings are potentially important in understanding the pathophysiology of vascular diseases, for example, atherosclerosis and restenosis following balloon angioplasty, where SMC migration is a contributing factor.
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PMID:Dynamic expression of alpha 1 beta 1 and alpha 2 beta 1 integrin receptors by human vascular smooth muscle cells. Alpha 2 beta 1 integrin is required for chemotaxis across type I collagen-coated membranes. 797 39

Magnesium status may be compromised with ageing for two reasons: insufficient intake (magnesium deficiency) or alterations in magnesium metabolism (magnesium depletion). There is a large volume of literature suggesting that magnesium deficit contributes to the ageing process and to the vulnerability to age-related diseases. One of the biological changes associated with ageing is an increase in free radical formation with subsequent damage to cellular processes. Prime targets of the more reactive free radicals are unsaturated lipids in cell membranes, amino acids in proteins, and nucleotides in DNA. The accumulation of unrepaired oxidative damage products may be a major factor in cellular ageing. Magnesium-deficient animals show an increased susceptibility to an in vivo oxidative stress and their tissues are more susceptible to in vitro peroxidation. Moreover, the protective properties of various antioxidant drugs and nutrients suggest that free radicals are involved in the injury process of magnesium deficiency. The consequences on stress susceptibility, defective membrane functions and perturbation of intracellular calcium metabolism, inflammation, cardiovascular diseases including atherosclerosis and ischaemia/reoxygenation injury, diabetes, fibrosis, immune dysfunction and other diseases associated with ageing are presented and discussed.
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PMID:Magnesium and ageing. I. Experimental data: importance of oxidative damage. 815 89

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.
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PMID:Magnesium and ageing. II. Clinical data: aetiological mechanisms and pathophysiological consequences of magnesium deficit in the elderly. 815 90

Abnormal dietary deficiency in Mg as well as abnormalities in Mg metabolism appear to play important roles as risk factors for ischemic heart disease and acute myocardial infarction, namely in hypertensive vascular disease, diabetic vascular disease, insulin resistance, atherosclerosis and vasospasm. Experimental, epidemiological as well as clinical evidence that supports a role for Mg in these risk factors are reviewed. Extracellular Mg ions ([Mg2+]o) exert important actions upon divalent cation metabolism, transport and intracellular release of [Ca2+]i and intracellular free Mg ([Mg2+]i) in both vascular smooth muscle and endothelial cells. Digital imaging microscopy, using molecular fluorescent probes, clearly indicates that both intracellular free Ca2+ and intracellular free Mg2+ are compartmented in both vascular smooth muscle cells and endothelial cells. [Mg2+]o appears to exert important effects on the precise subcellular location and concentration of both [Ca2+]i and [Mg2+]i. Use of specific ion-selective electrodes for [Mg2+]o has revealed that [Mg2+]o can change more rapidly than heretofore believed in cardiovascular pathophysiologic states. The latter new findings therefore suggest that the ionized level of [Mg2+]o is an important determinant of vascular tone, contractility and reactivity.
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PMID:Magnesium, hypertensive vascular diseases, atherogenesis, subcellular compartmentation of Ca2+ and Mg2+ and vascular contractility. 826 20

In this review, a rationale is presented for how hypercholesterolemia, hypertension, diabetes mellitus, end-stage renal disease, renal dialysis, and prolonged stress can all lead to atherosclerosis, ischemic heart disease, and stroke. The data indicate that Mg deficiency caused either by poor diet and/or errors in Mg metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Data from our laboratories and others indicate that reduction in extracellular and intracellular free Mg ions (Mg2+) can induce an entire array of pathophysiological phenomena known to be important in atherogenesis, that is, vasospasm, increased vascular reactivity, elevation in [Ca2+]i, formation of proinflammatory agents, oxygen radicals, platelet aggegation, reduction in cardiac bioenergetics, cardiac failure, oxidation of lipoproteins, gender-related modulation of endothelial-derived relaxing factor/NO, changes in membrane fatty acid saturation, changes in membrane plasmalogens and N-phospholipids (suggesting changes in intracellular phospholipid signals), and probably transcription factors.
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PMID:Magnesium and cardiovascular biology: an important link between cardiovascular risk factors and atherogenesis. 886 81

Magnesium is an essential cation for more than 300 enzymes in our body. Among them, it is a cofactor for ATP metabolism. Diverse clinical manifestations have been reported in conjunction with Mg++ deficiencies, including sudden death, accelerated atherosclerosis, asthma, neurologic and even psychiatric clinical entities. Limited previous studies with Mg++ supplementation have shown to be of a large preventive advantages. We summarize the current literature concerning Mg++ supplementation and recommend to do so on national basis adding magnesium to the water supplies of large areas.
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PMID:Magnesium fortification of water. A possible step forward in preventive medicine? 953 78


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