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 activity of hexokinase, dehydrogenases of pentose cycle, total lactate dehydrogenase, and cytochrome-C-oxidase level was determined in the aorta of rats with hyperthyroidism caused by the intraperitoneal administration of L-thyroxin. In the administration of hormone doses approaching the physiological ones there was an increase in the activity of cytochrome-C-oxidase and a tendency to the increase of 6-phosphogluconate dehydrogenase. Elevation of the activity of all the enzymes under study, excluding lactate dehydrogenase, and in increase of the amount of extractable protein occurred in the administration of moderate thyroxin doses. An increase of hexokinase and particularly of cytochrome-C-oxidase activity was revealed in hyperthyroidism with phenomena of thyrotoxicosis. The activity of the rest of the enzymes approached control. The data obtained are discussed from the point of view of the role played by thyroid hormones in the pathogenesis of atherosclerosis.
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PMID:[Effect of thyroxine on oxidative enzymatic activity in the rat aorta]. 21 88

Hypercholesterolemia plays an important role in the lipid abnormalities in chronic renal failure (CRF). It is thought to contribute to both a progression of renal failure and atherosclerosis. Despite intensive research, the etiopathogenesis of hypercholesterolemia in CRF patients is still obscure. The present study was designed to evaluate the possible role of cholesterol overproduction in the development of hypercholesterolemia associated with experimental CRF. We found that plasma total cholesterol and cholesterol distributed in VLDL, LDL and HDL concentrations were significantly enhanced in CRF rats. Simultaneously, the rate of liver cholesterol biosynthesis in vivo (measured by determining the incorporation of tritium from tritiated water intraperitoneally injected into cholesterol ), liver microsomal 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity and liver HMG-CoA reductase mRNA presence were elevated. Significant increases in activity of liver malic enzyme, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, NADPH-producing enzyme (required for cholesterol synthesis) have also been observed in CRF rats. In conclusion, the increased rate of liver cholesterol biosynthesis due to increase of HMG-CoA reductase and NADPH-producing enzyme gene expression could be one of the possible causes of hypercholesterolemia in CRF animals.
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PMID:Increased rate of cholesterologenesis--a possible cause of hypercholesterolemia in experimental chronic renal failure in rats. 1206 35

Native low-density lipoprotein (LDL) and oxidized LDL (oxLDL) possess a wide variety of biological properties, and play a central role in atherogenesis. In this study, we used a proteomic analysis of human monocyte THP-1 cells induced with oxLDL or with LDL, to identify proteins potentially involved in atherosclerotic processes. Of the 2500 proteins detected, 93 were differentially expressed as a result of priming with LDL or oxLDL. The proteins were unambiguously identified by comparing the masses of their tryptic peptides with those of all known proteins using MALDI-TOF MS and the NCBI database. The largest differences in expression were observed for vimentin (94-fold increase), meningioma-expressed antigen 6 (48-fold increase), serine/threonine protein phosphatase 2A (40-fold increase), and beta-1,3-galactosyltransferase (15-fold increase). In contrast, the abundance of an unnamed protein product and phosphogluconate dehydrogenase decreased 30-fold and 25-fold, respectively. The expression of some selected proteins was confirmed by Western blot and RT-PCR analyses. The proteins identified in this study are attractive candidates for further biomarker research. This description of the altered protein profiles induced by oxLDL in human monocytes will support functional studies of the macrophage-derived foam cells involved in the pathogenesis of atherosclerosis.
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PMID:Proteome analysis of human monocytic THP-1 cells primed with oxidized low-density lipoproteins. 1640 58