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)

The goal of the present research was to assess the efficacy of combination treatment with antioxidant coenzyme Q10 and simvastatin as well as coenzyme Q10 without statin therapy in order to prevent coronary atherosclerosis. 42 outpatients were divided into 2 groups: receiving coenzyme Q10 (Hasco-Lek, Poland) 60mg daily and its combination with simvastatin (zocor, vasilip) 10mg daily for an 8-week period. The treatment with coenzyme Q10 demonstrated its potential independent role in positive modification of oxidative stress, antiatherogenic fraction of lipid profile, atherogenic ratio, platelet aggregability. Taking into consideration the obtained results the study supports the use of coenzyme Q10 in combination with statins. Suggested attractive approach may result in complete correction of dislipidemia, reverse of endothelial dysfunction, reduce degree of oxidative stress and platelet aggregability. Consequently such a combination may be beneficial in preventing of further development of atherosclerosis in native coronary arteries as well as in bypass grafts in all coronary heart disease patients with or without myocardial revascularization.
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PMID:Prevention of coronary atherosclerosis by the use of combination therapy with antioxidant coenzyme Q10 and statins. 1582 19

Statins decrease LDL cholesterol and the risk of atherosclerotic cardiovascular disease (CVD). They also decrease coenzyme Q10 (CoQ10), an effect that may negate some of the statin benefit on CVD. We examined the relationship between plasma CoQ10 concentration and CVD in a prospective case-control study of the effect of pravastatin. Plasma samples from 250 LIPID trial patients who over 6 years suffered a recurrent CVD event (CVD death, nonfatal MI or stroke) and 250 matched controls who remained event-free for the same duration of follow-up were assayed for CoQ10 and lipids (cholesterol and cholesterylesters). Mean plasma CoQ10 concentrations were significantly lower in pravastatin-treated patients than in those assigned placebo (0.51 versus 0.60 micromol/L, P = 0.006), and there was a moderate correlation between CoQ10 and common cholesterylesters (Pearson correlation coefficients in patients randomised to placebo, range r = 0.42-0.63). Univariate conditional logistic regression did not suggest any relationship between plasma CoQ10 and the risk of future CVD events (odds ratio 1.18; 95% CI 0.74-1.87; P = 0.49). Instead, we observed a reduction in the rate of recurrent CVD events with increasing ratio of plasma cholesterylarachidonate to cholesteryllinoleate. This study confirms that pravastatin lowers plasma CoQ10 concentrations, but this does not appear to predict the risk of recurrent CVD events.
Atherosclerosis 2006 Jul
PMID:Neither plasma coenzyme Q10 concentration, nor its decline during pravastatin therapy, is linked to recurrent cardiovascular disease events: a prospective case-control study from the LIPID study. 1621 12

Several naturally occurring constituents have received considerable attention because of their potential antioxidant activity. Consuming a diet rich in natural antioxidants has been associated with prevention from and/or treatment of atherosclerosis. Bioactive components of food, which are of special interest, include the Vitamins E and C, polyphenols, carotenoids-mainly lycopene and beta-carotene, and coenzyme Q10, featured by antioxidant properties. Antioxidant therapy is supposed to be effective in the early stages of atherosclerosis by preventing LDL oxidation and the oxidative lesion of endothelium. This review focuses on the effect of dietary antioxidants pertained to LDL oxidation and to the vascular endothelial dysfunction. Now that the human genome has been completely sequenced, genetic factors involved in oxidation may open new horizons to identify persons at risk for cardiovascular disease, allowing effective dietary intervention strategies to recover normal homeostasis and to prevent diet-related implications. On this basis, current studies on the action of selected antioxidant nutraceuticals on the activity of transcription factors, such as final targets in the signal transduction cascade and gene regulation, may emerge into new treatment concepts.
Atherosclerosis 2006 Jul
PMID:Dietary antioxidants in preventing atherogenesis. 1631 12

A family of constitutive cell surface ECTO-NOX proteins capable of oxidizing reduced quinones, initially described as NADH oxidases, has offered an opportunity to formulate, for the first time, a complete electron transport chain from the cytosol to oxygen at the cell surface with the ECTO-NOX proteins acting as the terminal oxidases. The ECTO-NOX proteins of the cell surface have been postulated as well to link the accumulation of lesions in mitochondrial DNA to cell surface accumulations of reactive oxygen species as one consequence of their role as a terminal oxidase in a plasma membrane electron transport chain. Of the several ECTO-NOX proteins now known, one is a novel cell surface form (arNOX) associated with lymphocytes, sera, saliva and perspiration of patients of age 50 or older and is capable of directly reducing ferric cytochrome c through the generation of superoxide. Because of their cell surface location, ECTO-NOX proteins capable of superoxide generation in response to aging would serve to propagate the aging cascade both to adjacent cells and to oxidize circulating lipoproteins. The generation of superoxide associated with aging is inhibited by coenzyme Q10. As such, the findings provide a rational basis for the antiaging activity of circulating coenzyme Q10 in the prevention of atherosclerosis and other aging-related oxidative changes in cell membranes and circulating lipoproteins.
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PMID:Aging-related cell surface ECTO-NOX protein, arNOX, a preventive target to reduce atherogenic risk in the elderly. 1670 50

In order to assess efficacy of one of natural antioxidants--coenzyme Q10 (90 mg daily) and its combination with simvastatin (10 mg daily) 44 outpatients with coronary atherosclerosis were examined. Twenty four patients had undergone coronary artery bypass surgery, 12--coronary angioplasty and in 8 coronary heart disease was confirmed by angiography. Duration of treatment was 12 weeks. Positive effects of coenzyme Q10 was particularly expressed in relation to antiatherogenic fraction of cholesterol which increased by 23%. Index of atherogenicity decreased by 27%. At the background of coenzyme Q10 treatment 30% reduction in plasma lipoperoxide levels occurred demonstrating potentially independent role of coenzyme Q10 in positive modification of oxidative stress. Coenzyme Q10 revealed antiaggregatory ability. It was not related to the improvement of endothelial function. Normalization of plasma nitric oxide concentrations was achieved only with combination of coenzyme Q10 and simvastatin. This fact may be explained by positive action of statins on endothelial function.
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PMID:[Combination treatment with coenzyme Q10 and simvastatin in patients with coronary atherosclerosis]. 1704 94

Coenzyme Q10 (CoQ10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals produced during oxidative phosphorylation in the inner mitochondrial membrane. Oxidative stress, resulting in glutathione loss and oxidative DNA and protein damage, has been implicated in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury. Though most have tended to be pilot studies, there are published preliminary clinical trials showing that CoQ10 may offer promise in many brain disorders. For example, a 16-month randomized, placebo-controlled pilot trial in 80 subjects with mild Parkinson's disease found significant benefits for oral CoQ10 1,200 mg/day to slow functional deterioration. However, to date, there are no published clinical trials of CoQ10 in Alzheimer's disease. Available data suggests that oral CoQ10 seems to be relatively safe and tolerated across the range of 300-2,400 mg/day. Randomized controlled trials are warranted to confirm CoQ10's safety and promise as a clinically effective neuroprotectant.
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PMID:Coenzyme Q10: a review of its promise as a neuroprotectant. 1719 65

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Oxidative stress appears to play a pivotal role in atherosclerosis. Coenzyme Q10 (CoQ10), one of the most important antioxidants, is synthesized de novo by every cell in the body. Its biosynthesis decreases with age and its deficit in tissues is associated with degenerative changes of aging, thus implicating a possible therapeutic role of CoQl0 in human diseases. There is evidence to support the therapeutic value of CoQ10 as an adjunct to standard medical therapy in congestive heart failure. However, much further research is required, especially in the use of state-of-the-art techniques to assess functional outcomes in patients with congestive heart failure.
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PMID:Coenzyme Q10 supplementation and heart failure. 1760 5

The long-term efficacy and safety of HMG-CoA reductase inhibitors (statins) have been established in large multicenter trials. Inhibition of this enzyme, however, results in decreased synthesis of cholesterol and other products downstream of mevalonate, such as CoQ10 or dolichol. This was a randomized double-blind, placebo-controlled study that examined the effects of CoQ10 and placebo in hypercholesterolemic patients treated by atorvastatin. Eligible patients were given 10mg/day of atorvastatin for 16 weeks. Half of the patients (n=24) were supplemented with 100mg/day of CoQ10, while the other half (n=25) were given the placebo. Serum LDL-C levels in the CoQ10 group decreased by 43%, while in the placebo group by 49%. The HDL-C increment was more striking in the CoQ10 group than in the placebo group. All patients showed definite reductions of plasma CoQ10 levels in the placebo group, by 42%. All patients supplemented with CoQ10 showed striking increases in plasma CoQ10 by 127%. In conclusion atorvastatin definitely decreased plasma CoQ10 levels and supplementation with CoQ10 increased their levels. These changes in plasma CoQ10 levels showed no relation to the changes in serum AST, ALT and CK levels. Further studies are needed, however, for the evaluation of CoQ10 supplementation in statin therapy.
Atherosclerosis 2007 Dec
PMID:Effects of CoQ10 supplementation on plasma lipoprotein lipid, CoQ10 and liver and muscle enzyme levels in hypercholesterolemic patients treated with atorvastatin: a randomized double-blind study. 1768 47

This work, in addition to the peculiar medical aspects of the children obesity, synthesize the experimental findings about the main plasmatic antioxidants (uric acid, ascorbic acid, retinol, coenzyme Q10, lycopene) and the platelet fatty acids profile in groups of children according to the following BMI criteria: 43 with a BMI ranging between 25 and 29; 43 with a BMI ranging between 21.7 e 22.9 and 20 with a BMI ranging between 18.5 e 20; average age 10.49 +/- 2.66. The antioxidants show a particular behaviour: in fact they decrease according to the BMI recorded within the groups. About this issue the international literature is not consistent. Probably different results can be found in more severe condition of obesity. Another important result is for the platelet fatty acid, independently from the BMI, weight etc. compared to the other subjects. The difference found is for the stearic acid, from 15 to 21 point of percentage, compared to all the other groups investigated. In agreement with the international literature, stearic acid seems to have an important role in the control of the platelet activation. This finding, could offer a better possibility to understand the progression of the atherosclerosis towards the ischemic condition, according to the age. The utilisation of particular mathematic models, the Artificial Neural Network, beyond the normal advanced statistic methods, has open to the understanding of phenomena, otherwise, inexplicable. With the Artificial Neural Network (ANN) it has been possible to classify the children using the ANN map built for the depressive condition (platelet fatty acids markers: palmitic acid, linoleic acid, arachidonic acid) and the ANN map built for the ischemic condition (platelet fatty acids markers: oleic acid, linoleic acid, arachidonic acid). Examining the maps, a certain percentage of children seems to be at high risk for several psychiatric conditions with respect to the major depression, while for the ischemic pathology the children are in the same position of the ischemic subjects. Because we know that the children are not ischemic, probably they have the same biochemical characteristics but are protected by the high level of stearic acid and by the high degree of saturation of the platelets. For this reason, children cannot belong to the map area of the major depression, which, in turn, is characterized by a very high degree of unsaturation of the fatty acids. Further studies are needed to better understand the complex situation of the children from the biochemical and psychiatric point of view.
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PMID:[Childhood obesity: recent advances and an experimental contribution]. 1902 56

Coenzyme Q10 (ubiquinone) is a mitochondrial coenzyme which is essential for the production of ATP. Being at the core of cellular energy processes it assumes importance in cells with high energy requirements like the cardiac cells which are extremely sensitive to CoQ10 deficiency produced by cardiac diseases. CoQ10 has thus a potential role for prevention and treatment of heart ailments by improving cellular bioenergetics. In addition it has an antioxidant, a free radical scavenging and a vasodilator effect which may be helpful in these conditions. It inhibits LDL oxidation and thus the progression of atherosclerosis. It decreases proinflammatory cytokines and decreases blood viscosity which is helpful in patients of heart failure and coronary artery disease. It also improves ischemia and reperfusion injury of coronary revascularisation. Significant improvement has been observed in clinical and hemodynamic parameters and in exercise tolerance in patients given adjunctive CoQ10 in doses from 60 to 200 mg daily in the various trials conducted in patients of heart failure, hypertension, ischemic heart disease and other cardiac illnesses. Recently it has been found to be an independent predictor of mortality in congestive heart failure. It has also been found to be helpful in vertigo and Meniere-like syndrome by improving the immune system. Further research is going on to establish firmly its role in the therapy of cardiovascular diseases.
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PMID:Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Meniere-like syndrome. 1963 84


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