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)

Feeding of cholesterol-rich diet in male rabbits resulted in increased levels of cholesterol in plasma, aorta and liver and total lipids, phospholipids, free fatty acids in aorta and liver. Garlic supplementation to this diet suppressed these effects but their levels were still higher as compared to control rabbits. The plasma fibrinolytic activity which was decreased on cholesterol feeding was considerably increased when this diet was supplemented with garlic. There was increase in the activity of phospholipase in the cell-free supernatant of aorta and liver and decrease in the activity of cell-free supernatant NADH dehydrogenase of aorta when atherogenic diet was supplemented with garlic. Histopathological studies of aorta, liver and heart supported biochemical studies and indicated retardative effect of garlic on the development of atherosclerosis.
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PMID:Effect of garlic supplementation to cholesterol-rich diet on development of atherosclerosis in rabbits. 186 1

1. Atherosclerosis (AS) in rats displays important clinical similarities to human AS. 2. After the experimental model of AS in rat was established and using a proteomic approach, we compared the protein profiling of aorta tissues from healthy and AS rats. 3. Using two-dimensional electrophoresis (2-DE), over 1878 protein species were separated; among them, 1239 protein spots were matched between different gels with average matching rate of approximately 66%. Gel analysis and protein characterization have identified 58 protein spots whose abundance is significantly altered in AS rats. 4. By using matrix-associated laser desorption ionization time-of-flight mass spectrometer (MALDI-TOF-MS) and NCBInr database, 46 proteins were successfully identified. Among them, 18 proteins were of increased abundance in diseased tissues including a group of oxidization-related enzymes such as peroxiredoxin2 and NADH dehydrogenase Fe-S protein 6, components of inflammatory pathways such as lamin A, while 28 proteins were of decreased abundance in the diseased state, including CaM-KII inhibitory protein, transferring, fructose-bisphosphate aldolase. 5. We believe that these results would give insights into the cellular and molecular mechanisms involved in AS development and might lead to the discovery of novel diagnostic markers and new therapeutic opportunities.
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PMID:Proteomic analysis of rat aorta during atherosclerosis induced by high cholesterol diet and injection of vitamin D3. 1662 Feb 92

Somatic mutations of the human mitochondrial genome can be a possible determinant of atherosclerosis. To test this possibility, forty mitochondrial mutations were analyzed in the present study in order to see which of these mutations might be associated with atherosclerosis. Ten mitochondrial mutations belonging to mitochondrial genes MT-RNR1 (rRNA 12S); MT-TL1 (tRNA-Leu, recognizes UUR); MT-TL2 (tRNA-Leu, recognizes CUN); MT-ND1, MT-ND2, MT-ND5, and MT-ND6 (subunits 1, 2, 5, and 6, respectively, of NADH dehydrogenase); and MT-CYB (cytochrome b) were potentially associated with atherosclerosis. From 29% (2 of 7 aortic samples) upto 86% (6 of 7 aortic samples) of aortic samples had a significant difference between atherosclerotic plaques and unaffected tissue, with the respect to the level of heteroplasmy for each mutation. Further, the homogenates of affected and normal intimae of 22 aortas were compared to reveal the average level of heteroplasmy for the above-mentioned 10 mutations. For five mutations, the mean level of heteroplasmy was significantly different in atherosclerotic intimal homogenates in comparison with the unaffected tissue. These mutations were A1555G, C3256T, T3336C, G13513A, and G15059A. Thus, it was demonstrated that at least five mitochondrial mutations occurring in MT-RNR1, MT-TL1, MT-ND2, MT-ND5, and MT-CYB genes are associated with atherosclerosis.
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PMID:Mitochondrial mutations are associated with atherosclerotic lesions in the human aorta. 2299 26

With aim of detection the spectrum of mitochondrial DNA mutations in patients with carotid atherosclerosis from Moscow Region, we used a Roche 454 high-throughput sequencing of the whole mitochondrial genome. We have found that the presence of a number of homoplasmic mitochondrial DNA mutations in genes of 16S ribosomal RNA, subunits 2, 4, and 5 NADH dehydrogenase, subunits 1 and 2 cytochrome C oxidase, subunit 6 ATP-synthase, tRNA- Leu 2 and cytochrome B differed between conventionally healthy participants of the study and patients with carotid atherosclerosis. We also found heteroplasmic mutations, including insertions one or several nucleotides, that occurred more frequently in mitochondrial DNA of conventionally healthy participants of the study or patients with atherosclerotic lesions.
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PMID:Mutations of mitochondrial genome in carotid atherosclerosis. 2585 49

Atherosclerosis is a basis of development for many cardiovascular diseases, which are leading causes of death among people in the 21-st century. One of possible causes of atherosclerosis may be somatic mutations of human mitochondrial genome. In order to identify mutations associated with atherosclerosis, we analyzed 42 mitochondrial mutations found in various pathologies. The subject of the study were individuals who died as a result of an accident or a sudden death. The material for the investigation were segments of intima from 7 aortas both normal and with lipofibrous plaques. DNA was isolated by a method of phenol-chloroform extraction. PCR-fragments of DNA containing the region of investigated mutations were analyzed by an original method of quantitative assessment of mitochondrial genome mutant alleles. This method was developed in our laboratory on the basis of pyrosequencing technology. Statistical data processing was performed using IBM SPSS Statistics 21.0 and by bootstrap analysis. 40 of 42 studied mutations were heteroplasmic and two were homoplasmic according to the absence of a mutant allele in atherosclerosis. The developed method of direct quantitative assessment of mitochondrial genome mutant alleles helped us to find three new mutations: 652delG, 961delC and 5132insAA. It was found that 11 of mitochondrial mutations (652insG, T3336S, C3256T, G14459A, G14846A, G15059A, 652delC, A1555G, C5178A, G13513A and G12315A), belonging to eight mitochondrial genes: rRNA 12S, tRNA - Leu (codon recognition UUR) and tRNA - Leu (codon recognition CUN), subunit 1, 2, 5 and 6 of NADH dehydrogenase and cytochrome B are potentially associated with atherosclerosis, because from 29% (2 of 7 aortas) to 86% (6/7) investigated aortas have a significant difference in the heteroplasmy level of these mutations in lipofibrous plaques compared to normal aortic intima.
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PMID:[Association of mitochondrial genome mutations with lipofibrous plaques in human aortic intima]. 2622 85