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| 1 | Antioxidants,inflammation and cardiovascular disease显示文摘Multiple factors are involved in the etiology of cardiovascular disease(CVD). Pathological changes occur in a variety of cell types long before symptoms become apparent and diagnosis is made. Dysregulation of physiological functions are associated with the activation of immune cells,leading to local and finally systemic inflammation that is characterized by production of high levels of reactive oxygen species(ROS). Patients suffering from inflammatory diseases often present with diminished levels of antioxidants either due to insufficient dietary intake or,and even more likely,due to increased demand in situations of overwhelming ROS production by activated immune effector cells like macrophages. Antioxidants are suggested to beneficially interfere with diseases-related oxidative stress,however the interplay of endogenous and exogenous antioxidants with the overall redox system is complex. Moreover,molecular mechanisms underlying oxidative stress in CVD are not fully elucidated. Metabolic dybalances are suggested to play a major role in disease onset and progression. Several central signalingpathways involved in the regulation of immunological,metabolic and endothelial function are regulated in a redox-sensitive manner. During cellular immune response,interferon γ-dependent pathways are activated such as tryptophan breakdown by the enzyme indoleamine 2,3-dioxygenase(IDO) in monocyte-derived macrophages,fibroblasts,endothelial and epithelial cells. Neopterin,a marker of oxidative stress and immune activation is produced by GTP-cyclohydrolase Ⅰ in macrophages and dendritic cells. Nitric oxide synthase(NOS) is induced in several cell types to generate nitric oxide(NO). NO,despite its low reactivity,is a potent antioxidant involved in the regulation of the vasomotor tone and of immunomodulatory signaling pathways. NO inhibits the expression and function of IDO. Function of NOS requires the cofactor tetrahydrobiopterin(BH4),which is produced in humans primarily by fibroblasts and endothelial cells. Highly toxic peroxynitrite(ONOO-) is formed solely in the presence of superoxide anion(O2-). Neopterin and kynurenine to tryptophan ratio(Kyn/Trp),as an estimate of IDO enzyme activity,are robust markers of immune activation in vitro and in vivo. Both these diagnostic parameters are able to predict cardiovascular and overall mortality in patients at risk. Likewise,a significant association exists between increase of neopterin concentrations and Kyn/Trp ratio values and the lowering of plasma levels of vitamin-C,-E and-B. Vitamin-B deficiency is usually accompanied by increased plasma homoycsteine. Additional determination of NO metabolites,BH4 and plasma antioxidants in patients with CVD and related clinical settings can be helpful to improve the understanding of redox-regulation in health and disease and might provide a rationale for potential antioxidant therapies in CVD. | Harald Mangge Kathrin Becker Dietmar Fuchs Johanna M Gostner | 2014 | World Journal of Cardiology2014,6,6: | 25 |
| 2 | The microbiota is dispensable for the early stages of peripheral regulatory T cell induction within mesenteric lymph nodes显示文摘Intestinal Foxp3+regulatory T cell(Treg)subsets are crucial players in tolerance to microbiota-derived and food-borne antigens,and compelling evidence suggests that the intestinal microbiota modulates their generation,functional specialization,and maintenance.Selected bacterial species and microbiota-derived metabolites,such as short-chain fatty acids(SCFAs),have been reported to promote Treg homeostasis in the intestinal lamina propria.Furthermore,gut-draining mesenteric lymph nodes(mLNs)are particularly efficient sites for the generation of peripherally induced Tregs(pTregs).Despite this knowledge,the direct role of the microbiota and their metabolites in the early stages of pTreg induction within mLNs is not fully elucidated.Here,using an adoptive transfer-based pTreg induction system,we demonstrate that neither transfer of a dysbiotic microbiota nor dietary SCFA supplementation modulated the pTreg induction capacity of mLNs.Even mice housed under germ-free(GF)conditions displayed equivalent pTreg induction within mLNs.Further molecular characterization of these de novo induced pTregs from mLNs by dissection of their transcriptomes and accessible chromatin regions revealed that the microbiota indeed has a limited impact and does not contribute to the initialization of the Treg-specific epigenetic landscape.Overall,our data suggest that the microbiota is dispensable for the early stages of pTreg induction within mLNs. | Carolin Wiechers Mangge Zou Eric Galvez Michael Beckstette Maria Ebel Till Strowig Jochen Huehn Joern Pezoldt | 2021 | Cellular & Molecular Immunology2021,18,5: | 2 |
| 3 | Beyond cholesterol-inflam-matory cytokines,the key mediators in atherosclerosis显示文摘 | Mangge H Hubmann H Pilz S | 2004 | Clin Chem Lab Med2004,42,5: | 1 |
| 4 | Insulin is an independent correlate of plasma homocysteine levels in obese children and adolescents 显示文摘 | Gallistl S Sudi K Mangge H | 2000 | Diabetes Care2000,23,9: | 1 |
| 5 | Visfatin/pre-B-cell colony-enhancing factor:a protein with various suggested functions显示文摘 | Pilz S Mangge H Obermayer-Pietsch B | 2007 | J Endocrinol Invest2007,30,2: | 1 |
| 6 | Activation of the haemostatic system in children with juvenile rheumatoid arthritis correlates with diseases activity显示文摘 | Gallistl S Mangge H Neuwirth G | 1998 | Thromb Res1998,92,6: | 1 |
| 7 | Inflammation,adiponectin,obesity and cardiovascular risk显示文摘 | Mangge H Aimer G Truschnig-Wilders M | 2010 | Curr Med Chem2010,17,36: | 1 |
| 8 | Laboratory medicine for molecular imaging of atherosclerosis显示文摘 | Mangge H Almer G Stelzer I | 2014 | Clin Chim Acta2014,437,: | 1 |
| 9 | Early rheumatoid arthritis is associated with diminished numbers of thl cells in stimulated peripheral blood 显示文摘 | Mangge H Felsner P Herrmann J | 1999 | Immunobiology1999,200,2: | 1 |
| 10 | Inflammation, adiponectin, obesity and cardiovascular risk显示文摘 | Mangge H Almer G Truschnig-Wilders M | 2010 | Curr Med Chem2010,17,36: | 1 |
| 11 | Cystatin C an early indicator for incipient renal disease in rheumatoid arthritis显示文摘 | Mangge H Liebmann P Tanil H | 2000 | Clin Chim Acta2000,300,12: | 1 |
| 12 | Csystatin C, an early indicator for incipient renal disease in rbeumatoid arthritis显示文摘 | Mangge H iehmann P Tanil H | 2000 | Clin Chim Acta2000,300,12: | 1 |
| 13 | Csystatin C,an early indicator for incipient renal disease in rbeumatoid artbritis显示文摘 | MANGGE H IEBMANN P TANIL H | 2000 | Clin Chim Acta2000,300,122: | 1 |
| 14 | Cystatin C, an early indicator for incipient renal disease in rbeumatoid artbritis显示文摘 | Mangge H iebmann P Tanil H | 2000 | Clin Chim ACTA2000,300,12: | 1 |
| 15 | Nuchal thickness of subcutaneous adipose tissue is tightly associated with an increased LMW/total adiponectin ratio in obese juveniles显示文摘 | Mangge H Almer G Haj-Yahya S | | 0,,: | 1 |
| 16 | Adiponectin and Mortality in Patients Undergoing Coronary Angiography 显示文摘 | Pilz S Mangge H WeUnitz B | 2006 | J Clin Endocrinol Metab2006,91,11: | 1 |
| 17 | Low grade inflammation in juvenile obesity and type 1 diabetes associated with early signs of atherosclerosis 显示文摘 | Mangge H Schauenstein K Stroedter L | 2004 | Exp Clin Endocrinol Diabetes2004,112,7: | 1 |
| 18 | Uric acid indicates a high cardiovascular risk profile but is not closely associated with insulin resistance in obese adolescents显示文摘 | Mangge H Pilz S Haj-Yahya S | 2008 | Diabetes Care2008,31,4: | 1 |
| 19 | Fatel occlusive vessel disease in a patient with systemic juvenile idiopathic arthritis 显示文摘 | Mangge H Heinzl B Grubbauer HM | 2004 | J Rheumatol2004,31,2: | 1 |
| 20 | Inflammation, adiponectin, obesity and cardiovascular risk显示文摘 | Mangge H Almer G Truschnig-Wilders M | 2010 | Curr Med Chem2010,17,36: | 1 |