Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been proposed that iron depletion protects against cardiovascular disease. There is increasing evidence that one mechanism for this protection may involve a reduction in iron levels within atherosclerotic plaque. Large increases in iron concentration are seen in human atherosclerotic lesions in comparison to levels in healthy arterial tissue. In animal models, depletion of lesion iron levels in vivo by phlebotomy, systemic iron chelation treatment or dietary iron restriction reduces lesion size and/or increases plaque stability. A number of factors associated with increased arterial disease or increased cardiovascular events is also associated with increased plaque iron. In rats, infusion of angiotensin II increases ferritin levels and arterial thickness which are reversed by treatment with the iron chelator deferoxamine. In humans, a polymorphism for haptoglobin associated with increased cardiovascular disease is also characterized by increased lesional iron. Heme oxygenase 1 (HO1) is an important component of the system for mobilization of iron from macrophages. Human HO1 promoter polymorphisms causing weaker upregulation of the enzyme are associated with increased cardiovascular disease and increased serum ferritin. Increased cardiovascular disease associated with inflammation may be in part caused by elevated hepcidin levels that promote retention of iron within plaque macrophages. Defective retention of iron within arterial macrophages in genetic hemochromatosis may explain why there is little evidence of increased atherosclerosis in this disorder despite systemic iron overload. The reviewed findings support the concept that arterial plaque iron is a modifiable risk factor for atherogenesis.
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PMID:Iron in arterial plaque: modifiable risk factor for atherosclerosis. 1861 22

Chronic inflammation is the cause of malnutrition and cardiovascular disease in hemodialysis patients. The purpose of this study was to assess C Reactive Protein (CRP) as an inflammatory marker and to define the relationship between CRP and other inflammatory and nutritional factors in this group of patients. One hundred and fourteen hemodialysis patients undergoing chronic dialysis (3 times a week for at least 4 hours) in two hemodialysis centers were enrolled in this cross-sectional study. Anthropometric and laboratory data including CRP, Il-6, hemoglobin, serum ferritin, triglyceride, cholesterol, albumin, total protein and transferrin were measured. The Kt/V for adequacy of dialysis was also calculated. There was a statistically significant correlation between the mean CRP and albumin, hemoglobin, and transferrin; while such relation was not found with BMI, ferritin, the length of dialysis, triceps skin fold thickness, mid arm circumference, mid arm muscle circumference, and Kt/V. We conclude that the negative relationship between CRP and albumin, transferrin, and hemoglobin suggests a correlation between inflammatory and nutritional factors.
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PMID:Chronic inflammation increases risk in hemodialysis patients. 1871 Dec 96

Given the reported association of cardiac complications with hereditary hemochromatosis and the high carrier frequency of HFE gene mutations in the natural population, it seems reasonable that such mutations might appear more frequently than expected among symptomatic cardiac patients. Thus, H63D, C282Y, and S65C mutations and their possible associations were examined in 477 Caucasian males undergoing coronary angiography. Genotypes were analyzed for differences between ferritin and transferrin levels, coronary artery disease (CAD), cardiomyopathy (CM), and cardiovascular disease (CVD) mortality. No significant differences were found in ferritin levels between those with or without HFE mutations (C282Y P = 0.632, H63D P = 0.765, S65C P = 0.568, and HFE mutation P = 0.568); however, there was a significant difference (P = 0.005) in mean transferrin levels between those with (252 microg/l) and without (275 microg/l) C282Y. No relationship between HFE mutations and CAD (C282Y, P = 0.402; H63D, P = 0.112; S65C, P = 0.170) or CVD death (C282Y, P = 0.560; H63D, P = 0.682; S65C, P = 0.664) was demonstrated using logistic regression. However, an association between S65C and CM was found (odds ratio 4.4; 95% confidence interval 1.3-13.3, P = 0.018). This suggests that the S65C allele may contribute to the development of CM, but that these three HFE mutations do not appear to play a significant role in development of ischemic heart disease.
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PMID:HFE mutations in heart disease. 1881 May 84

The principal causes of morbidity and mortality in children with chronic renal failure on maintenance hemodialysis are cardiovascular complications. Recently, it has been suggested that oxidative stress, chronic inflammation and malnutrition are risk factors for cardiovascular disease. However, to date, biomarkers of oxidative stress have not been well studied in children. The aim of this study was to investigate the relationship between oxidative stress and cardiovascular risk factors in children on hemodialysis therapy. Twenty-eight hemodialysis patients (13 females, 15 males; mean age 15.1 +/- 2.5 years) and 20 healthy children (13 females, seven males; mean age 14.3 +/- 2.7 years) were included in the study. Levels of antibodies to oxidized low-density lipoprotein (oLABs), high sensitivity C-reactive protein (hs-CRP), albumin, prealbumin, transferrin, and ferritin were measured. Antibodies to oxidized low-density lipoprotein (LDL) in hemodialysis patients were lower than those in the controls (P < 0.05). The patients with lower oLAB titers had higher levels of hs-CRP and ratio of erythropoietin to hematocrit (EPO/Htc), and lower levels of albumin, prealbumin, apolipoprotein A-1 (ApoA(1)), and high-density lipoprotein (P < 0.05). Antibodies to oxidized LDL in hemodialysis patients with dyslipidemia were lower than those of patients with normal lipid profile (P < 0,05). This study showed that children treated by hemodialysis are exposed to oxidative stress and chronic inflammation. We suggest that oLAB levels are decreased in children on hemodialysis as a result of severe oxidative stress and that these antibodies are related to inflammation, anemia, malnutrition and dyslipidemia.
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PMID:Oxidative stress in children on hemodialysis: value of autoantibodies against oxidized low-density lipoprotein. 1895 4

The 'iron hypothesis' claims that Fe depletion protects against IHD. The objective of the present study was to investigate the associations between serum ferritin levels and the risk of CVD and IHD in a population-based sample. A total of 2874 subjects with serum ferritin levels between 15 and 300 microg/l from the Danish part of the 'Monitoring of Trends and Determinants in Cardiovascular Disease' (DAN-MONICA) I study and the 1914 Cohort survey were followed for 10 years. Information on behavioural and socio-demographic characteristics were collected and serum ferritin levels measured. Non-fatal and fatal CVD and IHD were identified by the International Classification of Diseases diagnoses numbers. Multivariable Cox proportional hazard regression models with restricted cubic splines were performed. During the follow-up period, 310 subjects (201 men; 109 women) and 161 subjects (117 men; forty-four women) experienced CVD and IHD, respectively. Our analyses revealed no statistically significant associations between serum ferritin levels and the risk of CVD or IHD in both sexes. However, in women, the results argue for a U-shaped relationship between serum ferritin levels and CVD as well as IHD. In concordance with former prospective studies, the present results do not support the hypothesis that normal body Fe stores should play a significant role in the development of CVD.
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PMID:Is serum ferritin within the reference range a risk predictor of cardiovascular disease? A population-based, long-term study comprising 2874 subjects. 1920 21

Hemodialysis (HD) patients suffer from chronic inflammations which make them at increased risk of cardiovascular diseases. The purpose of this study was to see if there is a significant association between inflammatory factors such as ferritin and C-reactive protein (CRP) as well as troponin T in patients on HD. We assessed these serum factors as well as other known cardiac risk factors in 53 patients on HD. The serum ferritin and CRP levels were measured by chemiluminescence's immune assay while troponin T levels were measured by electrochemist luminescence immune assay. We found that serum concentrations of CRP and ferritin were not significantly higher in patients on HD with known cardiac risk factors (compared with the control group) (p< 0.05). However, the serum troponin T levels in HD patients with cardiovascular risk factors were significantly higher than the control group. Our study suggests that elevated serum troponin T levels can play an important role as a predictor of cardiovascular disease in HD patients. Also, inflammatory factors such as CRP and ferritin may be influenced by chronic inflammation or nutritional status of these patients.
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PMID:Assessment of inflammatory factors and cardiac troponin T in hemodialysis patients. 1923 7

Modern medicine has greatly benefited from recent dramatic improvements in imaging techniques. The observation of physiological events through interactions manipulated at the molecular level offers unique insight into the function (and dysfunction) of the living organism. The tremendous advances in the development of nanoparticulate molecular imaging agents over the past decade have made it possible to noninvasively image the specificity, pharmacokinetic profiles, biodistribution, and therapeutic efficacy of many novel compounds. Several types of nanoparticles have demonstrated utility for biomedical purposes, including inorganic nanocrystals, such as iron oxide, gold, and quantum dots. Moreover, natural nanoparticles, such as viruses, lipoproteins, or apoferritin, as well as hybrid nanostructures composed of inorganic and natural nanoparticles, have been applied broadly. However, among the most investigated nanoparticle platforms for biomedical purposes are lipidic aggregates, such as liposomal nanoparticles, micelles, and microemulsions. Their relative ease of preparation and functionalization, as well as the ready synthetic ability to combine multiple amphiphilic moieties, are the most important reasons for their popularity. Lipid-based nanoparticle platforms allow the inclusion of a variety of imaging agents, ranging from fluorescent molecules to chelated metals and nanocrystals. In recent years, we have created a variety of multifunctional lipid-based nanoparticles for molecular imaging; many are capable of being used with more than one imaging technique (that is, with multimodal imaging ability). These nanoparticles differ in size, morphology, and specificity for biological markers. In this Account, we discuss the development and characterization of five different particles: liposomes, micelles, nanocrystal micelles, lipid-coated silica, and nanocrystal high-density lipoprotein (HDL). We also demonstrate their application for multimodal molecular imaging, with the main focus on magnetic resonance imaging (MRI), optical techniques, and transmission electron microscopy (TEM). The functionalization of the nanoparticles and the modulation of their pharmacokinetics are discussed. Their application for molecular imaging of key processes in cancer and cardiovascular disease are shown. Finally, we discuss a recent development in which the endogenous nanoparticle HDL was modified to carry different diagnostically active nanocrystal cores to enable multimodal imaging of macrophages in experimental atherosclerosis. The multimodal characteristics of the different contrast agent platforms have proven to be extremely valuable for validation purposes and for understanding mechanisms of particle-target interaction at different levels, ranging from the entire organism down to cellular organelles.
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PMID:Nanoparticulate assemblies of amphiphiles and diagnostically active materials for multimodality imaging. 1943 19

Iron-induced cardiovascular disease is the leading cause of death in iron-overloaded patients. Deferasirox is a novel, once daily oral iron chelator that was recently approved for the treatment of transfusional iron overload. Here, we investigate whether deferasirox is capable of removing cardiac iron and improving iron-induced pathogenesis of the heart using the iron overload gerbil model. Animals were randomly divided into three groups: control, iron overload, and iron overload + deferasirox treatment. Iron-dextran was given 100 mg/kg per 5 days i.p for 10 weeks. Deferasirox treatment was taken post iron loading and was given at 100 mg/kg/day p.o for 1 or 3 months. Cardiac iron concentration was determined by inductively coupled plasma atomic emission spectroscopy. Compared with the untreated group, deferasirox treatment for 1 and 3 months decreased cardiac iron concentration 17.1% (P = 0.159) and 23.5% (P < 0.05), respectively. These treatment-associated reductions in cardiac iron were paralleled by decreases in tissue ferritin expression of 20% and 38% at 1 and 3 months, respectively (P < 0.05). Using oxyblot analysis and hydroethidine fluorescence, we showed that deferasirox significantly reduces cardiac protein oxidation and superoxide abundance by 36 and 47.1%, respectively (P < 0.05). Iron-induced increase in oxidative stress was also associated with increased phosphorylation of ERK-, p38-, and JNK-mitogen-activated protein kinase (MAPK). Interestingly, deferasirox treatment significantly diminished the phosphorylation of all three MAPK subfamilies. These results suggest that deferasirox may confer a cardioprotective effect against iron induced injury.
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PMID:Deferasirox removes cardiac iron and attenuates oxidative stress in the iron-overloaded gerbil. 1965 Jan 17

Specific recommendations for anemic individuals consist in increasing red meat intake, but the population at large is advised to reduce consumption of red meat and increase that of fish, in order to prevent the risk of developing cardiovascular disease. This study aimed to determine the effects of consuming an oily fish compared to a red meat diet on iron status in women with low iron stores. The study was designed attending the Consolidated Standards of Reporting Trials (CONSORT) statement guidelines. It was a randomised crossover dietary intervention study of two 8-week periods. Twenty-five young women with low iron stores completed the study. Two diets containing a total of 8 portions of fish, meat and poultry per week were designed differing only in their oily fish or red meat content (5 portions per week). At the beginning and the end of each period blood samples were taken and hemoglobin, hematocrit, serum ferritin, serum iron, serum transferrin, serum transferrin receptor-2 and the Zn-protoporphyrin/free-protoporphyrin ratio were determined. Food intake and body weight were monitored. During the oily fish diet, PUFA intake was significantly higher (p=0.010) and iron intake lower (mean+/-SD, 11.5+/-3.4 mg/day vs. 13.9+/-0.1 mg/day, p=0.008), both diets providing lower mean daily iron intake than recommended for menstruating women. Although there were no significant differences after 16 weeks, serum ferritin moderately decreased and soluble transferrin receptor increased with the oily fish, while changes with the red meat diet were the opposite. In conclusion, an oily fish diet compared to a red meat diet does not decrease iron status after 8 weeks in iron deficient women.
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PMID:Iron status biomarkers in iron deficient women consuming oily fish versus red meat diet. 1988 95

Although the iron-heart disease hypothesis is prevalent, the epidemiological findings are incongruent. The relationship of serum ferritin with early cardiovascular disease (CVD), particularly atherosclerosis, has not been evaluated extensively, particularly with accounting for inflammation. We examined this association in a case-control study of 124 age- and sex-matched pairs embedded in the population-based random sample (MONICA survey) in Southwest France, taking into account inflammation status. Cases had >or=2 carotid atherosclerotic plaques and controls had none. Inflammation was assessed using several markers, including serum alpha-1 acid glycoprotein (AGP) and high sensitivity C-reactive protein. There was an interaction of inflammation with group (case/control) for serum ferritin. In adults without elevated AGP, serum ferritin was significantly greater in atherosclerotic cases than in adults in the control group. In models adjusted for CVD risk factors, the odds of atherosclerosis increased with the increase in serum ferritin in individuals without elevated AGP; for every 10-microg/L increase in serum ferritin, the risk for atherosclerosis increased by 3% (odds ratio [95% CI]: 1.03 [1.01-1.06]). In conclusion, carotid atherosclerosis was positively associated with serum ferritin in individuals free from subclinical inflammation based on AGP. Further prospective and/or experimental studies are needed to corroborate the observed association of iron status with atherosclerosis.
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PMID:Iron status is associated with carotid atherosclerotic plaques in middle-aged adults. 2018 83


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