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 research projects of the European Forum on Antiphospholipid Antibodies are representative of how dynamic is this area of investigation. The present review is focused on the most recent projects of the Forum on the aetiopathogenic aspects of the antiphospholipid syndrome (APS). Studies on the genetic background of the APS are ongoing in order to better define the proximity between APS and full-blown systemic lupus erythematosus. However, the analysis of the polymorphisms of genes coding for inflammatory mediators may offer new information on the role of inflammatory processes in triggering thrombotic events as well as the whole susceptibility for developing the vascular manifestations. A systematic and wide detection of serological markers of infectious processes will give new insight on the role of infectious agents in favouring autoimmunity in APS. Owing to the well-known role of vitamin D(3) defect in autoimmune disease, the detection of vitamin plasma levels in APS patients will offer the rationale for a possible therapeutic supplementation. Additional projects are aimed to better characterize the diagnostic/prognostic value of antiphospholipid antibodies (aPL) by defining their epitope specificity and binding avidity. Pregnancy complications represent the obstetric side of APS. Research projects are focussed on the role of complement activation in placenta damage and on the potential ability of aPL to affect the fertility. Finally, a study has been planned in order to draw definitive conclusions on the associations between aPL and atherosclerosis.
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PMID:European Forum on Antiphospholipid Antibodies: research in progress. 1967 94

Long-term survival after successful renal transplantation is shortened by cardiovascular disease. Cardiovascular disease is a main cause of morbidity and death among children and young adults after renal transplantation. The aim of our study was to measure the carotid intima media thickness (cIMT) and determine its relationship to the risk factors for early arteriopathy in renal transplant recipients. Sixty-six stable renal transplant patients (36 female and 30 male), 7-25 years of age (mean 18.3 +/- 4.5 years) were enrolled in this study. The cIMT was measured by high-resolution B mode ultrasonography in multiple projections. The results were correlated with clinical and paraclinical parameters, including age, gender, body mass index (BMI), blood pressure, glomerular filtration rate (GFR), duration of dialysis, duration of chronic kidney disease (CKD), post-transplantation interval, calcium-phosphate (CaxP) product, cumulative dose of Ca-based P binder and calcitriol, lipid profile, uric acid, and cyclosporine level. The mean post-transplantation follow-up period was 64 +/- 40 months. The mean cIMT standard deviation score (SDS) of the patients and the control group was 0.60 +/- 0.81 mm (range -1.10 mm to 2.75 mm) and -1.25 +/- 0.95 mm (range -3.23 mm to 0.26 mm), respectively. Renal transplant recipients had a significantly greater cIMT than that of the controls (P < 0.001). Among several risk factors, there were positive correlations between cIMT SDS and gender, and cumulative dose of calcitriol (P = 0.02 and P = 0.02, respectively). In conclusion, subclinical atherosclerosis is present in young transplant recipients. Non-invasive monitoring of cIMT in renal transplant patients for the detection of early vascular lesions might be of value in preventing cardiovascular disease. Further studies are needed to see if proper monitoring of vitamin D therapy before and after transplantation could be helpful in the prevention of arteriopathy in renal transplant recipients.
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PMID:Subclinical atherosclerosis and related risk factors in renal transplant recipients. 1991 Dec 1

Endothelial lipase (EL) is a major determinant of HDL metabolism and associated with the development of atherosclerosis, however the regulated expression of EL in atherosclerosis is unclear. In this study, we investigated EL expression in rat atherosclerosis and explored the potential mechanisms regulating EL expression by employing LPS on Raw264.7 cells in vitro. Rat atherosclerosis model was established fed on high-cholesterol diet (HCD) combined with vitamin D(2) (VD). Western blotting and immunochemistry staining revealed that EL expression was increased in the aorta, especially the atherosclerotic lesions in HCD rats. LPS increased EL expression in a time and dose dependent manner in Raw264.7 cells and NFkappaB inhibitor, PDTC attenuated the effects of LPS on EL. EMSA revealed that LPS stimulated NFkappaB binding to EL promoter. In summary, EL was upregulated in rat atherosclerosis and LPS stimulates EL expression in vitro through NFkappaB activation.
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PMID:Regulated expression of endothelial lipase in atherosclerosis. 1993 48

Growth hormone-releasing peptides (GHRP) and ghrelin are synthetic and natural ligands of growth hormone secretagogue receptor (GHSR) respectively and are shown to exert protective actions on cardiac dysfunction. Because ghrelin has been reported to inhibit proinflammatory responses in human endothelium and GHSR has been identified in blood vessels, we hypothesized that GHRP could alleviate the development of atherosclerosis (As). Atherosclearosis was induced by a short period (4 days) of vitamin D(3) and chronic (three months) intragastric feeding of high fat emulsion (containing 0.5% propylthiouracil) in adult SD rats. Some As rats received chronic hexarelin (a variant of GHRP) injection (SC BID, 30 days) and normal rats received placebo as control. Significant atherosclerosis developed in animals fed with the emulsion. Serum total cholesterol and LDL-c increased, and HDL-c and aortic nitric oxide (NO) decreased significantly in As group. Hexarelin suppressed the formation of atherosclerotic plaques and neointima, partially reversed serum HDL-c/LDL-c ratio and increased the levels of serum NO and aortic mRNAs of eNOS, GHSR and CD36 in As rats. Hexarelin also decreased [(3)H]-TdR incorporation in cultured vascular smooth muscle cell (VSMC) and calcium sedimentation in aortic wall. Furthermore, foam cell formation induced by ox-LDL was decreased by hexarelin. In conclusion, hexarelin suppresses high lipid diet and vitamin D3-induced atherosclerosis in rats, possibly through upregulating HDL-c/LDL-c ratio, vascular NO production and downregulating the VSMC proliferation, aortic calcium sedimentation and foam cell formation. These novel anti-atherosclerotic actions of hexarelin suggest that the peptide might have a clinical potential in treating atherosclerosis.
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PMID:Hexarelin suppresses high lipid diet and vitamin D3-induced atherosclerosis in the rat. 1993 84

During the aging process, remodeling of several body systems occurs, and these changes can have a startling effect upon the immune system. The reduction in sex steroids and growth hormones and declines in vitamin D concentration that accompany the aging process are associated with increases in the baseline levels of inflammatory proteins. At the same time, inflammation arising from atherosclerosis and other chronic diseases further contributes to the inflammatory milieu and effects a state of chronic inflammation. This chronic inflammation, or ''inflammaging'' as it has been termed, seems to be associated with a host of adverse effects contributing to many of the health problems that increase morbidity and decrease both quality of life and the ability to maintain independence in old age. For nurses to be truly informed when caring for older people and to ensure that they have a detailed understanding of the complexities of older people's health needs, they must have a knowledge of the physiological and immunological changes with age. This is the first of a two-part article on inflammatory processes in aging. These age-related changes are presented here, including an examination of the impact of genetic and lifestyle factors. The effect of these changes on the health of the individual and implications for practice are described in Part 2.
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PMID:Inflammation in aging part 1: physiology and immunological mechanisms. 1993 11

End-stage renal disease (ESRD) is associated with both accelerated cardiovascular disease and alterations in vitamin D and mineral metabolism. Calcification of both coronary and extra-cardiac vessels is common in ESRD. Several studies suggest that vascular calcification is associated with coronary atherosclerosis, vascular wall stiffness, left ventricular hypertrophy, and subsequent increased mortality, but it is not yet clear if vascular calcification is a direct cause of these changes or merely a marker of disease. Reviewed here is the current state of research on the biology and the significance of vascular calcification in ESRD, the role of vitamin D therapy in its development, and options for management.
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PMID:Vascular calcification and ESRD: a hard target. 1999 90

Vitamin D deficiency results in abnormal mineralization of bones and has resulted in prevention programs for children with supplementation when they are breast fed. Further activities of vitamin D relate to defence of microbial infections, e.g. tuberculosis, prevention of cancer, contractility of muscle cells and counteraction of congestive heart failure. Given early reports in the 1960s on deleterious effects of vitamin D supplementation in rodents, that is ectopic media ossification of arterial vessels, a pro-atherogenic function had been anticipated for humans as well. However, cross-sectional studies reveal that vitamin D deficiency in humans is associated with elevated blood pressure and propagation of atherogenesis. These contradictory findings on the progression of atherosclerosis may be reconciled by dissecting the activation mechanism(s) of vitamin D in rodents versus humans. Notably, novel findings convincingly indicate that vitamin D exerts anti-inflammatory effects. In conclusion, vitamin D supplementation in adults may be regarded as simple means with few potential side effects to prevent atherogenesis or halt its progression and combat arterial hypertension. Adjustment of vitamin D dosing regimens is required in patients with chronic kidney disease; however, prospective clinical trials are urgently needed to guide these recommendations with evidence.
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PMID:Vitamin D and cardiovascular risk. 2003 26

Osteoporosis and vascular disease are commonly found together in elderly people. Several common mechanisms and risk factors have been suggested to contribute to the development of osteoporosis and atherosclerosis. The present cross-sectional study was performed to determine whether the degree of bone turnover is correlated to carotid intima-media thickness (CCA-IMT), as a marker of subclinical atherosclerosis. We selected 50 outpatients (mean age 71.7 +/- 12.3), underwent to eco-Doppler evaluation of extracranial carotid tract, without history of calcium and/or vitamin D supplementation, or antireabsorptive therapy. CCA-IMT was measured by high-resolution B-mode ultrasonography. Bone turnover was evaluated by analysing serum levels of C-terminal telopeptide of type I collagen (sCTX), and bone-specific alkaline phosphatase. We also evaluated the vitamin D status by determination of the serum concentration of 25-hydroxyvitamin D [25(OH)D]. We found a prevalence of hypovitaminosis D [serum 25(OH)D levels <30 ng/mL, mean value 10.7 +/- 5.8] of 91.8%, and an increased bone resorption, with mean sCTX levels higher than reference values (mean 1.18 +/- 0.57 ng/mL). A significant positive correlation was found between CCA-IMT and age (r = 0.480, P = 0.001), erythrocyte sedimentation rate (ESR: r = 0.438, P = 0.001), high-sensitivity C-Reactive Protein (HsCRP: r = 0.482, P = 0.011), serum creatinine (r = 0.305, P = 0.031), and sCTX (r = 0.389, P = 0.006). In a multivariate linear regression, CCA-IMT was independently predicted by age (beta = 0.34, P = 0.001), ESR (beta = 0.37, P = 0.005), and sCTX (beta = 0.32, P = 0.006). The preliminary results of our study seem to indicate that after adjustment for established cardiovascular risk factors, sCTX independently predict an increased CCA-IMT in the elderly population.
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PMID:Carotid intima-media thickness and bone turnover: the role of C-terminal telopeptide of type I collagen. 2018 21

There is increasing evidence for health benefits accomplished by activated vitamin D through interaction with the vitamin D receptor (VDR) that go beyond calcium and bone homeostasis and regulation of parathyroid hormone (PTH) secretion. Treatment with vitamin D receptor agonists (VDRAs) is associated with reduced mortality in (pre)dialysis patients. Interestingly, these relations are independent of PTH levels and calcium x phosphorus product. This suggests the presence of biological functions of vitamin D that are independent of its interaction with the parathyroid glands. Because chronic kidney disease leads to increased cardiovascular mortality, mechanisms in which VDRAs can influence cardiovascular disease are discussed. These mechanisms comprise the potential ameliorating effects of VDRAs on atherosclerosis, arterial media calcification, cardiac hypertrophy, the renin-angiotensin system and thrombosis. Moreover, treatment strategies with VDRAs are discussed together with several recent observational studies. Treatment advice consists of correction of 25(OH) vitamin D deficiency, low-dose calcitriol in patients with secondary hyperparathyroidism, and activated vitamin D analogues may be indicated when higher doses are needed to suppress PTH secretion. New insights into biological and clinical effects of VDRAs may broaden the patient group that may benefit from VDRA treatment to patients with creatinine clearances in the 30 to 60 ml/min range.
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PMID:Role of vitamin D in cardiovascular disease. 2030 5

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). In type 2 diabetics, the prevalence of vitamin D deficiency is 20% higher than in non-diabetics, and low vitamin D levels nearly double the relative risk of developing CVD compared to diabetic patients with normal vitamin D levels. However, the mechanism(s) by which vitamin D deficiency leads to an increased susceptibility to atherosclerosis in these patients is unknown. We studied the effects of vitamin D replacement on macrophage cholesterol metabolism and foam cell formation in obese, hypertensive diabetics and non-diabetic controls. We found that 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] suppressed foam cell formation by reducing acetylated low density lipoprotein (AcLDL) and oxidized low density lipoprotein (oxLDL) cholesterol uptake in diabetics only. 1,25(OH)2D3 downregulation of c-Jun N-terminal kinase activation reduced PPARgamma and CD36 expression, and prevented oxLDL-derived cholesterol uptake. In addition, 1,25(OH)2D3 suppression of macrophage endoplasmic reticulum stress improved insulin signaling, downregulated SR-A1 expression, and prevented oxLDL- and AcLDL-derived cholesterol uptake. The results of this research reveal novel insights into the mechanisms linking vitamin D signaling to foam cell formation in diabetics and suggest a potential new therapeutic target to reduce cardiovascular risk in this population.
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PMID:Vitamin D regulates macrophage cholesterol metabolism in diabetes. 2033 38


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