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)

Lipoprotein lipid analysis has been carried out in 39 women and 28 men with chronic renal failure on haemodialysis. The results have been analysed in relation to the etiology of the renal disease and compared with those obtained in age- and sex-matched controls and in triglyceride-matched controls. Serum cholesterol was normal or low in glomerulonephritis but was normal in analgesic nephropathy. Serum triglycerides and VLDL lipids were raised uniformly regardless of the etiology of the renal disease. LDL triglyceride and HDL triglyceride were also raised. LDL cholesterol and phospholipid were low in glomerulonephritis but were normal in analgesic nephropathy. HDL cholesterol was reduced in both male and female patients regardless of etiology, statistical significance was not reached for the women. The ratio of esterified to free cholesterol tended to be reduced in all the lipoproteins regardless of sex or etiology but the changes were not significant in all groups. Comparison of the lipid abnormalities with those found in other hyperlipidaemic states suggests that the lipid disorders found in chronic renal failure are probably insufficient to explain the rapid development of vascular disease which has been reported.
Atherosclerosis 1979 Dec
PMID:Lipoprotein lipids in chronic renal failure and haemodialysis. The influence of etiology and implications for atherogenesis. 22 78

Autoimmune hyperlipidemia (AIH) may be induced a variety of antibodies which inhibit different stages of the lipolytic process by which the lipid load is removed from the circulating lipoproteins. In a patient having a monoclonal gammopathy and a nephrotic syndrome with a glomerulonephritis and a marked hypertriglyceridemia, it was found previously that the monoclonal IgG gamma Lac. reacted with human VLDL as well as with human serum albumin. Here it is demonstrated that the purified IgG gamma inhibits the lipolysis of triglyceride substrates by reacting with a substance (Lac. S) necessary for lipoprotein lipase activity. The interaction of IgG lambda Lac. with serum or HDL-activated triglyceride substrates inhibits the lipolytic activity of human and rat plasma post heparin and also adipose tissue lipases. It slightly inhibits the activity of swine pancreatic lipases. The Lac S. which reacts with IgG Lac. is associated to whole and delipidated VLDL and HDL and not to LDL or purified APo-A. It may be an Apo-C or a non-peptidic co-factor of the lipases which remains bound to the apoprotein core after delipidation. Its lack of species specificity and its presence as traces in HSA preparations favors the latter hypothesis. The Lac. substances is different from the Pg and As substances which were found to react with IgA anti-Pg and IgG anti-As antibodies in previously reported antilipoprotein AIH.
Atherosclerosis 1977 Jan
PMID:Inhibition of lipoprotein lipase activity by a monoclonal immunoglobulin in autoimmune hyperlipidemia. 83 49

A spontaneously hypercholesterolemic male rat, found in the Sprague-Dawley strain, was mated with normocholesterolemic females of the same strain: the male offspring were hypercholesterolemic. By selecting rats according to their plasma cholesterol levels and repeated brother-sister mating, progeny became progressively more hypercholesterolemic--especially the males--when fed a basal low-cholesterol diet. These rats were tentatively given the short name of SHC and have at present been bred to the F14 generation. Hypercholesterolemia in male SHC rats proceeded in two stages: plasma cholesterol rose only slightly during the first stage up to the age of about 10 weeks and then increased progressively in the subsequent stage. Female SHC rats developed a high degree of hypercholesterolemia from the age of 10 months. SHC rats maintained on the basal diet were not obese, but their kidneys and livers enlarged. Histological examination showed that glomerulonephritis developed in the kidney of male SHC rats by the age of 9 months. The liver of these rats was not fatty and contained rather less lipid than usually found in the normal Sprague-Dawley rat. Male and female SHC rats were subjected to gonadectomy at the age of 4 weeks, and were then maintained on the basal diet for 18 weeks. Blood cholesterol was higher throughout the experiment in ovariectomized female SHC rats than in controls, and the renal lesion was correspondingly worse. However, gonadectomy in male SHC rats had no effect on the disease.
Atherosclerosis 1977 Jun
PMID:Serum and tissue lipids and glomerulonephritis in the spontaneously hypercholesterolemic (SHC) rat, with a note on the effects of gonadectomy. 90 16

The nephrotic syndrome is characterized by proteinuria, hypoalbuminemia and hypercholesterolemia. Hypercholesterolemia is in some cases a risk factor for atherosclerosis in this group of patients. The lipid plasma spectrum was studied in 45 patients with the nephrotic syndrome. Most pronounced changes of the lipid composition of the plasma were revealed in patients with systemic lupus erythematosus and a special form of mesangio-proliferative glomerulonephritis which is characterized by a torpid course and rapid development of chronic renal failure. Plasma atherogenicity was calculated according to the index of plasma atherogenicity. A high atherogenicity index was revealed in patients with an association of the nephrotic syndrome and arterial hypertension. Plasma atherogenicity is determined mainly by the level of high-density-lipoprotein cholesterol.
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PMID:[Lipidemia in the nephrotic syndrome and the atherogenicity of the plasma]. 145 41

Platelet-derived growth factor (PDGF), a potent mitogen for mesenchymal cells in culture, is expressed in vivo in a variety of inflammatory conditions associated with cell proliferation, including atherosclerosis, wound repair, pulmonary fibrosis, and glomerulonephritis. However, it is not known if PDGF mediates the fibroproliferative responses that characterize these inflammatory disorders. We administered neutralizing anti-PDGF IgG or control IgG to rats with mesangial proliferative nephritis. Inhibition of PDGF resulted in a significant reduction in mesangial cell proliferation, and largely prevented the increased deposition of extracellular matrix associated with the disease. This suggests that PDGF may have a central role in proliferative glomerular disease.
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PMID:Inhibition of mesangial cell proliferation and matrix expansion in glomerulonephritis in the rat by antibody to platelet-derived growth factor. 156 7

Oxidant injury has been implicated in the pathogenesis of inflammatory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likely to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.
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PMID:Reactive oxygen molecules, oxidant injury and renal disease. 166 82

A study was made of the regularities and changes in the fatty acid spectrum of total lipids of the blood serum, in interaction of carbohydrate lipid metabolism, and in the hypophyseal and thyroid system in 92 patients with the nephrotic form of acute and chronic glomerulonephritis. It has been discovered that the nephrotic form of glomerulonephritis is marked by a complex of changes in the fatty acid spectrum of the blood serum, in carbohydrate lipid metabolism at the sites of their conjunction, and in the hypophyseal and thyroid system which can be regarded as metabolic potentialities of atherosclerosis formation.
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PMID:[Biochemical markers of atherogenesis in a nephrotic form of glomerulonephritis in children]. 175 21

Endothelin, originally identified as a vasoconstrictive peptide derived from vascular endothelial cells, is now known to exert diverse biological effects on a wide variety of tissues and cell types through its own receptor(s). One of the outstanding actions of endothelin is a cell growth promoting activity which is demonstrated in several cell types including cultured vascular smooth muscle cells, fibroblasts, glomerular mesangial cells and osteoblasts. The mitogenic effect is likely mediated by stimulation of phospholipase C via receptor-G-protein coupling, and subsequent activation of protein kinase C. The effect of endothelin may contribute to the cell-proliferation response under various physiological and pathological conditions, such as wound healing and development of atherosclerosis and glomerulonephritis. Recently, three distinct endothelin-related genes have been cloned, suggesting that mammals, including humans, produce three members of this peptide family, endothelin (ET)-1 (the 'classical' endothelin), ET-2 and ET-3, which may act on distinct subtypes of endothelin receptor to induce different cellular responses.
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PMID:Endothelin, its diverse biological activities and mechanisms of action. 249 Dec 62

Using a computed image analyser, coronary arteries from 50 autopsied patients with systemic lupus erythematosus (SLE) were examined on the three vessels (RCA, LAD, LCX) and compared with those of age-matched controls. The intima of coronary artery was significantly thickened much more in the case of SLE than in the case of age-matched controls. This was statistically significant (p less than 0.01). Hypertension and glomerulonephritis did not but corticosteroid therapy had an influence on the development of intimal thickening ratio of the coronary arteries in SLE patients. The mean intimal thickening ratio of the coronary arteries in the patients with SLE and without corticosteroid therapy was larger than that of patients with corticosteroid therapy (p less than 0.1). It appears possible to conclude that inflammatory change of SLE itself is one of the promoting factors of coronary atherosclerosis.
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PMID:Coronary atherosclerosis in patients with systemic lupus erythematosus at autopsy. 357 64

A review of 51 patients who died while enrolled in a long-term prospective study of systemic lupus erythematosus (SLE) revealed that active SLE may persist or reappear late in the course of the disease. Vascular events, especially atherosclerotic coronary artery disease, occurred frequently. Moderate to severe atherosclerosis was seen in patients who had died of any cause after a prolonged duration of the disease and often contributed significantly to death. Diffuse proliferative glomerulonephritis, CNS lupus and major infections were indications of poor prognosis particularly early in its course.
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PMID:Mortality in systemic lupus erythematosus: the bimodal pattern revisited. 401 45


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