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)

Some of the genetic factors and environmental factors such as diet and drug therapies that are known to increase the risk of hyperlipidemia and possibly the predisposition to cardiovascular disease are reviewed. The cholesterol associated with the low-density lipoproteins (LDL), accounting for 60-75% of the plasma levels, is responsible for the powerful and direct relationship which exists between plasma cholesterol and coronary heart disease. Also, the cholesterol that accumulates in atheromatous lesions is derived primarily from plasma LDL. Hyperlipidemia is defined by elevated levels of the plasma levels; the risk for atherosclerosis is associated with the classification types IIa, IIb, III, and possibly IV, a classification system based on phenotypic manifestations of increased lipoprotein fractions. The Lipid Research Clinics Program reports data on plasma lipid and lipoprotein cholesterol distributions of a large-scale screening of white men and women (both with and without sex hormone usage) aged 20-59 years in the US. They found age-related trends for rising triglycerides and cholesterol with differences between the sexes clearly demonstrated. It has been established that normolipemic individuals are not immune to the development of atherosclerosis. The recent focus on the apolipoprotein moieties has revealed a number of normolipemic dyslipoproteinemias associated with tissue lipid infiltration. Multifactorial population studies provide a strong case for the powerful role of the environment, i.e., predominantly dietary intake of total fat, saturated fat, saturated fats, and calories, in hyperlipidemia. According to the Seven Countries Study, populations with higher levels of cholesterol and LDL cholesterol (and increased atherosclerosis) have saturated fat intakes of 10% or more of calories. Migration studies of Japanese populations in Japan and in the US also show the influence of diet. As was shown early on, oral contraceptive (OC) use predisposes to the development of hyperlipidemia. OCs also predispose to other cardiovascular risk factors that, when combined with smoking, bring about a greatly magnified risk for myocardial infarction. Also reviewed in terms of their effect on the lipoprotein profile are antihypertensive therapies, retinoids, and hypolipidemic agents. Regarding genetic predisposition, single-gene mutations in apoproteins, lipoproteins, and some of the enzymes involved in lipoprotein may underlie disorders of hyperlipoproteinemia or hypolipoproteinemia.
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PMID:Risks for hyperlipidemia. 287 33

For decades, research interest has focused on hypertriglyceridemia and hypercholesterolemia, because of their association with atherosclerosis. Recently, however, increasing attention has been paid to rare hypolipidemic states that can cause adverse consequences in young patients. Studies of genetic disorders of fat transport have afforded new insights into the mechanisms involved in intestinal lipid handling and lipoprotein metabolism. This article reviews briefly the current state of knowledge about inherited lipoprotein deficiencies, including abetalipoproteinemia, hypobetalipoproteinemia and chylomicron retention disease. These disorders share many common characteristics: they all cause fat malabsorption, low levels of circulating lipids and fat-soluble vitamins, failure to thrive in early childhood, ataxic neuropathy and visual impairment. However, their etiology is genetically different. Abetalipoproteinemia is caused by the absence of microsomal transfer protein, whereas hypobetalipoproteinemia is due to defects in the apolipoprotein B gene. The etiopathogenesis of chylomicron retention disease is as yet unexplained. Research on these rare, inherited fat disorders of absorption will continue to provide significant advances in our understanding of human physiology and may yield novel therapeutic approaches to atherosclerosis.
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PMID:The genetic basis of primary disorders of intestinal fat transport. 888 69

Atherosclerosis is a disease with a chronic-progressive course. We report on the statistic prevalence of vascular lesions in 1,500 asymptomatic patients with vascular diseases examined with Computed Tomography (CT) for different reasons. The aortoiliac arterial district was involved in 934/1,500 patients (62.3%), with simple or calcified plaques, thrombosis or dilatations. We investigated the involvement of other arterial vessels (47%) whenever feasible (57.7% of cases). The aorta was thrombosed in 107 patients (2.8%) and the thrombus associated with a calcification and a dilated vessel in 45 of them (42.1%). The aorta or the iliac arteries were enlarged in 62 patients (4.1%) and arterial diameter exceeded 4 cm in 20 patients (1.3%). Finally, the statistical significance was analyzed considering risk factors-i.e., smoking, arterial hypertension, diabetes and hypolipoproteinemia. All the patients with 2 or more risk factors had positive CT findings; the prevalence was 75% in cigarette smokers, 83% in hypertensive, 81.3% in dislipidemic and 93.5% in diabetic patients. These data demonstrate that, in agreement with international literature reports, it is possible to single out the groups of patients that, because of their age, risk factors and sex, should be considered for color Doppler screening programs and the selected cases to be submitted to CT.
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PMID:[Assessment of "occasional" atherosclerotic lesions identified with computerized tomography. Analysis of tomodensitrometric findings and identification of "risk" groups in 1,500 patients]. 938 Aug 73

LDs (lipid droplets) carrying TAG (triacylglycerol) and cholesteryl esters are emerging as dynamic cellular organelles that are generated in nearly every cell. They play a key role in lipid and membrane homoeostasis. Abnormal LD dynamics are associated with the pathophysiology of many metabolic diseases, such as obesity, diabetes, atherosclerosis, fatty liver and even cancer. Chylomicrons, stable droplets also consisting of TAG and cholesterol are generated in the intestinal epithelium to transport exogenous (dietary) lipids after meals from the small intestine to tissues for degradation. Defective chylomicron formation is responsible for inherited lipoprotein deficiencies, including abetalipoproteinaemia, hypobetalipoproteinaemia and chylomicron retention disease. These are disorders sharing characteristics such as fat malabsorption, low levels of circulating lipids and fat-soluble vitamins, failure to thrive in early childhood, ataxic neuropathy and visual impairment. Thus understanding the molecular mechanisms governing the dynamics of LDs and chylomicrons, namely, their biogenesis, growth, maintenance and degradation, will not only clarify their molecular role, but might also provide additional indications to treatment of metabolic diseases. In this review, we highlight the role of two small GTPases [ARFRP1 (ADP-ribosylation factor related protein 1) and ARL1 (ADP-ribosylation factor-like 1)] and their downstream targets acting on the trans-Golgi (Golgins and Rab proteins) on LD and chylomicron formation.
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PMID:Trans-Golgi proteins participate in the control of lipid droplet and chylomicron formation. 2303 2