Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Molecular tools are rapidly elucidating the molecular and cellular processes underlying myocardial infarction. To further understand these biological processes in vivo, investigators are embracing the burgeoning field of molecular imaging. Here we review important aspects of molecular imaging technology and then devote the majority of the text to studies that shed light on the in vivo pathogenesis of myocardial infarction. In particular, we focus on post-infarction healing and remodeling and discuss molecular imaging of proteolytic activity, angiogenesis, transglutaminase activity, and apoptosis. In the future, novel reporter agents and high-resolution cardiac imaging systems should enable imaging of emerging targets such as activated macrophages and myeloperoxidase activity, as well as stem cell-based and gene therapy-based myocardial regenerative strategies, in both experimental and clinical subjects.
J Mol Cell Cardiol 2006 Dec
PMID:Molecular imaging of myocardial infarction. 1706 33

Oxidative damage to lipids and proteins is an important component of atherosclerotic cardiovascular disease (CVD). Studies of oxidation-related molecules are helping to define atherosclerotic mechanisms, and measurements of circulating levels of specific oxidant compounds may improve cardiovascular risk assessment. The present article reviews accumulating data of selected oxidative biomarkers that support their role in providing diagnostic and/or prognostic information. For example, plasma levels of the enzyme myeloperoxidase, which generates the strong oxidizing agent hypochlorous acid, have been found to be correlated with risk for myocardial infarction and endothelial dysfunction. Elevated levels of lipoprotein-associated phospholipase A(2) are associated with coronary artery disease (CAD) and stroke. Oxidized phospholipids play an important role in atherosclerosis. Recent studies measuring circulating levels of oxidized phospholipids have suggested a strong association with CAD, plaque disruption, and response to 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor ("statin") therapy. Isoprostanes correlate strongly with cardiovascular risk factors, but their role in risk prediction is less well defined. Future studies are expected to clarify the role of oxidative biomarkers in the diagnosis and prognosis of CVD and to determine their value in specific clinical populations.
Am J Cardiol 2006 Dec 04
PMID:Oxidative biomarkers in the diagnosis and prognosis of cardiovascular disease. 1712 79

Although anti-IL-6-mAb down-regulates cardiac IL-6 and attenuates IL-6-mediated cardiac dysfunction following trauma-hemorrhage, it is not known whether blockade of IL-6 receptor will down-regulate cardiac IL-6 and improve cardiac function under those conditions. Six groups of male adult rats (275-325 g) were used: sham/trauma-hemorrhage+vehicle, sham/trauma-hemorrhage+IgG, sham/trauma-hemorrhage+anti-rat sIL-6R. Rats underwent trauma-hemorrhage (removal of 60% of the circulating blood volume and fluid resuscitation after 90 min). Vehicle (V), normal goat IgG or anti-rat sIL-6R (16.7 microg/kg BW) was administered intra-peritoneally in the middle of resuscitation. Two hours later, cardiac function was measured by ICG dilution technique; blood samples collected, cardiomyocytes isolated, and cardiomyocyte nuclei were then extracted. Cardiac IL-6, IL-6R, gp130, IkappaB-alpha/P-IkappaB-alpha, NF-kappaB, and ICAM-1 expressions were measured by immunoblotting. Plasma IL-6 and cardiomyocyte NF-kappaB DNA-binding activity were determined by ELISA. In additional animals, heart harvested and cardiac MPO activity and CINC-1 and -3 were also measured. In another group of rats, cardiac function was measure by microspheres at 24 h following trauma-hemorrhage. Cardiac function was depressed and cardiac IL-6, P-IkappaB-alpha, NF-kappaB and its DNA-binding activity, ICAM-1, MPO activity, and CINC-1 and -3 were markedly increased after trauma-hemorrhage. Moreover, cardiac dysfunction was evident even 24 h after trauma-hemorrhage. Administration of sIL-6R following trauma-hemorrhage: (1) improved cardiac output at 2 h and 24 h (p<0.05); (2) down-regulated both cardiac IL-6 and IL-6R (p<0.05); and (3) attenuated cardiac P-IkappaB-alpha, NF-kappaB, NF-kappaB DNA-binding activity, ICAM-1, CINC-1, -3, and MPO activity (p<0.05). IgG did not significantly influence the above parameters. Thus, IL-6-mediated up-regulation of cardiac NF-kappaB, ICAM-1, CINC-1, -3, and MPO activity likely contributes to altered cardiac function following trauma-hemorrhage. Since IL-6R blockade after trauma-hemorrhage down-regulates cardiac IL-6 and improves cardiac functions, blockade of IL-6R following trauma-hemorrhage appears to be a novel and effective adjunct for improving organ and cell function under those conditions.
J Mol Cell Cardiol 2007 Mar
PMID:Anti-rat soluble IL-6 receptor antibody down-regulates cardiac IL-6 and improves cardiac function following trauma-hemorrhage. 1731 58

Oxidative stress is common in inflammatory processes of many diseases, including the Chagas' disease, which is characterized by chronic inflammation. The present study is a sequence of a related publication [Oliveira TB, Pedrosa RC, Wilhelm Filho D. Oxidative stress in chronic cardiopathy associated with Chagas' disease. Int J Cardiol in press.] on the same subjects, which showed an increase in oxidative stress associated with the progression of the severity of the disease. Components of the antioxidant system and oxidative biomarkers present in the blood were measured in the same chronic chagasic patients (n=40), before and after vitamin E (800 IU/day) and vitamin C (500 mg/day) supplementation for 6 months. Antioxidant enzymes and contents of reduced glutathione in erythrocytes and plasma TBARS contents were analyzed in four groups of patients in different stages of chronic Chagas heart disease (n=10 each group, groups I, II, III, and IV) according to the Los Andes classification. After the combined vitamin supplementation, TBARS and protein carbonyl levels were decreased in plasma, whilst red cell GSH contents were increased in group I. The vitamin E contents found in the plasma were inversely related to the severity of the disease. No differences in gamma-glutamiltransferase activities were detected but the myeloperoxidase levels were decreased in patients at the initial stages, whilst seric nitric oxide levels were increased in groups II and III. After the antioxidant supplementation, CAT activity was increased in group II, GPx activity was increased in group I, GR activity was increased in groups I and II, whilst the GST activity was decreased in groups II, III and IV. The results clearly indicate that the antioxidant supplementation was able to counteract the progressive oxidative stress associated with the disease. New perspectives for the treatment of Chagas' disease might include an antioxidant therapy in order to attenuate the consequences of oxidative insult related to this disease.
Int J Cardiol 2007 Dec 15
PMID:Antioxidant therapy attenuates oxidative stress in chronic cardiopathy associated with Chagas' disease. 1732 77

Baseline plasma myeloperoxidase (MPO) levels have been shown to independently predict the early risk of myocardial infarction (MI) in patients presenting with chest pain. In addition, baseline MPO levels have been demonstrated to predict the development of adverse cardiac events up to 6 months after an acute coronary syndrome (ACS). However, in contrast to other biomarkers, there are no data about the long-term independent predictive value of baseline MPO values in patients with ACS. The present study investigated the long-term prognostic significance of baseline MPO levels in a well-characterized cohort of 193 men with ACS who were referred for coronary angiography at a Veterans Administration Medical Center. All patients were followed prospectively for the development of death and MI, and follow-up data were available for all patients at 24 months. After controlling for different baseline clinical, laboratory, and angiographic variables, baseline plasma MPO values were a strong and independent predictor of MI at 24 months by multivariate analysis. Using the median MPO value of the entire cohort of patients (i.e., 20.34 ng/ml) as a prespecified cutoff, the MI-free survival at 24 months for the group whose baseline MPO values were < or =20.34 ng/ml was 88% compared with 74% in those whose values were >20.34 ng/ml (p = 0.0249 by log-rank test). In conclusion, these data demonstrate that baseline MPO levels independently predict MI at 2 years in patients with ACS.
Am J Cardiol 2007 May 15
PMID:Usefulness of baseline plasma myeloperoxidase levels as an independent predictor of myocardial infarction at two years in patients presenting with acute coronary syndrome. 1749 61

Hereby we report our observations derived from a pilot-study of 39 subjects (30 patients with coronary artery disease [CAD] and 9 non-CAD controls). In this work, we aimed to evaluate MPO-ANCA titer in the human coronary circulation for the first time; and examine its possible association with CAD and some cytokines/inflammatory markers. We found higher mean coronary MPO-ANCA titer in CAD subjects than in non-CAD controls; beside significant positive correlations between MPO-ANCA titers and both C-reactive protein and interleukin-6 levels. Thus, we might suggest the possible involvement of MPO-ANCA in coronary atherogenesis indirectly through modulating some pro-inflammatory cytokines/markers; that a large-scale study of MPO-ANCA in CAD patients may be warranted in the future.
Int J Cardiol 2008 Aug 01
PMID:A pilot-controlled study of myeloperoxidase-specific anti-neutrophil cytoplasmic autoantibody (MPO-ANCA) in the coronary circulation. 1765 36

The cellular injury that results from irreversible ischemia leads to the alteration of tissue function responsible for the phenomenon that we call left ventricular remodeling. Oxidative stress and inflammation are key elements of this process; in mice as in humans, elevation of markers of inflammation at the time of myocardial infarction (MI) is a predictor of the development of ischemic myopathy and of adverse clinical outcomes. Several leukocyte-derived enzyme systems are responsible for the release of oxidizing agents into the myocardium after ischemic injury and provide a means of better understanding MI. By identifying the oxidation products present after inflammation, the responsible leukocyte-generating oxidant systems can be elucidated. Interestingly, a key leukocyte-derived marker, myeloperoxidase (MPO), was formerly measured routinely by older-generation hematology analyzers. Patients with lower levels of MPO were noted to be at lower risk for untoward cardiovascular events, suggesting that humans are more genomically "hardwired" than previously thought. Studies with genetic knockout mice confirm the importance of these leukocyte-generated oxidants in the pathophysiologic consequences of ischemia. This clearly affects the anatomic extent of damage, the hemodynamic consequences, and ultimately, the clinical correlates and potential outcomes. An understanding of these oxidative processes and their relation to inflammation will be extremely useful in the development and understanding of potential therapeutic agents.
Am J Cardiol 2008 May 22
PMID:The role of leukocyte-generated oxidants in left ventricular remodeling. 1847 71

Over the last decade, significant data has accumulated to suggest that biomarkers of oxidative stress accurately reflect the presence of cardiovascular risk factors, the extent of cardiovascular disease (CVD), and cardiovascular outcomes. This cumulative evidence has supported the approval of several of these biomarkers for clinical applications. For example, lipoprotein-associated phospholipase A(2) (Lp-PLA2) and myeloperoxidase (MPO) mass assays are now available to assist clinicians in determining overall cardiovascular risk in asymptomatic patients thought to be at increased risk or in patients with cardiovascular symptoms. However, it is not yet firmly established whether and to what extent these oxidative biomarkers reflect changes in response to therapeutic interventions. This article reviews the latest data on MPO, isoprostanes, oxidized low-density lipoprotein, oxidized phospholipids, and Lp-PLA2 biomarker assays, and it assesses their role in reflecting therapeutic interventions to treat CVD.
Am J Cardiol 2008 May 22
PMID:In vivo markers of oxidative stress and therapeutic interventions. 1847 72

Inflammation plays a critical role in acute myocardial infarction. One inflammatory marker is myeloperoxidase (MPO). Its role as a predictor of in-hospital death in patients with ST-segment elevation myocardial infarction (STEMI) presenting with cardiogenic shock (CS) is unclear. Therefore, the aim of this study was to investigate the role of MPO as a predictor of in-hospital death in patients with STEMIs presenting with CS and treated with primary percutaneous coronary intervention. In 38 consecutive patients with CS complicating STEMIs who were treated with primary percutaneous coronary intervention, serum MPO levels were measured at coronary care unit admission using a commercially available enzyme-linked immunosorbent assay. The primary study end point was in-hospital cardiac death. Among the 38 patients included in the study, 20 died during their coronary care unit stays, whereas 18 survived. Compared with patients who survived, patients who died showed, at coronary care unit admission, higher serum MPO levels (81 +/- 28 vs 56 +/- 23 ng/ml, p <0.006). After controlling for different baseline clinical, laboratory, and angiographic variables, baseline serum MPO level was an independent predictor of in-hospital mortality on multivariate analysis (odds ratio 3.9, 95% confidence interval 1.8 to 7.5, p <0.001). In conclusion, admission MPO concentration is an independent predictor of in-hospital mortality in patients with STEMIs presenting with CS.
Am J Cardiol 2008 Jun 01
PMID:Prognostic value of admission myeloperoxidase levels in patients with ST-segment elevation myocardial infarction and cardiogenic shock. 1848 29

Takayasu's arteritis has often been difficult to diagnose because of a lack of typical symptoms and other specific makers. We report here a case of Takayasu's arteritis in a 73-year-old man who was considered to exhibit isolated pulmonary artery involvement. Pulmonary hypertension and right heart failure and severe stenosis in the main trunk and left pulmonary artery were observed. There was nothing remarkable in his routine blood-sample tests other than increased CRP and ESR. There were neither infectious nor collagen diseases. Anti-cardiolipin antibody, Antiphospholipid Syndrome, PR3-ANCA and MPO-ANCA were negative. We diagnosed the patient as having Takayasu's arteritis based on chronic inflammation and the morphologic features of pulmonary artery lesion. However, other large vessels and the aorta were not involved. Treatment was started with glucocorticoids. The symptoms gradually improved, and pulmonary artery pressure estimated by echocardiography decreased along with inflammatiory markers. There were no remarkable changes in the stenotic lesions in the pulmonary artery but the flow limit in the left pulmonary artery was improved.
J Cardiol 2008 Jun
PMID:Isolated pulmonary arterial stenosis caused by Takayasu's arteritis in an elderly male. 1852 95


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