0000000000461570

AUTHOR

Sven Wassmann

showing 5 related works from this author

Stimulation of the AT2 receptor reduced atherogenesis in ApoE−/−/AT1A−/− double knock out mice

2012

AT1 receptor blockers (ARB) and in part ACE inhibitors (ACI) potentially exert beneficial effects on atherogenesis independent of AT1 receptor inhibition. These pleiotropic effects might be related to angiotensin II mediated activation of the AT2 receptor. To analyze this hypothesis we investigated the development of atherosclerosis and the role of ACIs and ARBs in apolipoprotein E-deficient (ApoE(-/-)) mice and in ApoE/AT1A receptor double knockout mice (ApoE(-/-)/AT1A(-/-)). ApoE(-/-) mice and ApoE(-/-)/AT1A(-/-) mice were fed cholesterol-rich diet for 7 weeks. Vascular oxidative stress, endothelial dysfunction, and atherosclerotic lesion formation were evident in ApoE(-/-) mice, but were…

MaleApolipoprotein ERamiprilmedicine.medical_specialtyApolipoprotein BReceptor expressionGene ExpressionAngiotensin-Converting Enzyme InhibitorsBlood PressureAngiotensin II Type 2 Receptor BlockersIn Vitro TechniquesReceptor Angiotensin Type 2Receptor Angiotensin Type 1MiceApolipoproteins EInternal medicinemedicineAnimalsReceptorMolecular BiologyMice KnockoutAngiotensin II receptor type 1biologyChemistryAtherosclerosisLipidsAngiotensin IIMice Inbred C57BLOxidative StressEndocrinologybiology.proteinBlood Vesselslipids (amino acids peptides and proteins)Inflammation MediatorsTelmisartanCardiology and Cardiovascular Medicinehormones hormone substitutes and hormone antagonistsmedicine.drugJournal of Molecular and Cellular Cardiology
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Clinical review: impact of statin substitution policies on patient outcomes.

2009

Background. The increasing awareness of cost issues in health care has led to the increasing use of policy-driven substitution of branded for generic medications, particularly relative to statin treatment for cardiovascular diseases. While there are potential short-term health care savings, the consequences for primary care are under-researched. Our objective was to review data on intensive statin therapy and generic substitution in patients at high cardiovascular risk. Results. Current treatment guidelines for the prevention of cardiovascular disease are consistent in their recommendations regarding statin therapy and treatment targets. Clinical trials demonstrate that to reduce cardiovasc…

medicine.medical_specialtyStatinCost effectivenessmedicine.drug_classDiseasePlaceboReimbursement MechanismsRisk FactorsHealth caremedicineDrugs GenericHumanscardiovascular diseasesIntensive care medicinebusiness.industryPublic healthHealth Policynutritional and metabolic diseasesGeneral MedicineClinical trialEuropeCardiovascular DiseasesPractice Guidelines as TopicPhysical therapyObservational studylipids (amino acids peptides and proteins)Hydroxymethylglutaryl-CoA Reductase Inhibitorsbusiness
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Inhibition of Rac1 GTPase Decreases Vascular Oxidative Stress, Improves Endothelial Function, and Attenuates Atherosclerosis Development in Mice

2021

Aims: Oxidative stress and inflammation contribute to atherogenesis. Rac1 GTPase regulates pro-oxidant NADPH oxidase activity, reactive oxygen species (ROS) formation, actin cytoskeleton organization and monocyte adhesion. We investigated the vascular effects of pharmacological inhibition of Rac1 GTPase in mice.Methods and Results: We treated wild-type and apolipoprotein E-deficient (ApoE−/−) mice with Clostridium sordellii lethal toxin (LT), a Rac1 inhibitor, and assessed vascular oxidative stress, expression and activity of involved proteins, endothelial function, macrophage infiltration, and atherosclerosis development. LT-treated wild-type mice displayed decreased vascular NADPH oxidase…

RHOAInflammationVascular permeabilityfree radicalsPharmacologyCardiovascular Medicinemedicine.disease_causeActin cytoskeleton organizationendothelial functionmedicineoxidative stressDiseases of the circulatory (Cardiovascular) systemddc:610Endothelial dysfunctionOriginal Researchchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseGTPasesbiologymedicine.diseasechemistryatherosclerosis endothelial function oxidative stress free radicals Rac1 GTPasesRC666-701biology.proteinmedicine.symptomatherosclerosisCardiology and Cardiovascular MedicineOxidative stressRac1Frontiers in Cardiovascular Medicine
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NADPH Oxidase Accounts for Enhanced Superoxide Production and Impaired Endothelium-Dependent Smooth Muscle Relaxation in BKβ1 −/− Mice

2006

Objective— Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca 2+ -activated K + channels (BK). A regulatory BKβ1 subunit confers Ca 2+ , voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the β1-subunit. Methods and Results— Vascular superoxide in BKβ1 −/− was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity a…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxideMicechemistry.chemical_compoundSuperoxidesInternal medicineCyclic GMP-Dependent Protein KinasesmedicineAnimalsHumansProtein IsoformsNADH NADPH OxidoreductasesLarge-Conductance Calcium-Activated Potassium ChannelsMice KnockoutNADPH oxidasebiologySuperoxideMicrofilament ProteinsNADPH OxidasesPhosphoproteinsMolecular biologyVasodilationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseNAD(P)H oxidaseNOX1ApocyninNADPH Oxidase 1biology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseCell Adhesion MoleculesSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

2005

Objective— Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. Methods and Results— C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary training on running wheels (6 weeks). Inactivity increased vascular lipid peroxidation to 148±9% and upregulated superoxide release to 176±17% (L-012 chemiluminescence) and 188±29% (cytochrome C reduction assay), respectively. ROS production was predominantly increased in the endothelium and the medi…

rac1 GTP-Binding Proteinmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIArteriosclerosisNitric Oxide Synthase Type IIBiologymedicine.disease_causechemistry.chemical_compoundMiceApolipoproteins EInternal medicinePhysical Conditioning AnimalmedicineAnimalsNADH NADPH OxidoreductasesRNA MessengerEndothelial dysfunctionLife Stylechemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseSuperoxideNeuropeptidesNADPH Oxidase 1NADPH Oxidasesmedicine.diseasePhosphoproteinsMice Mutant Strainsrac GTP-Binding ProteinsMice Inbred C57BLVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologychemistryNOX1biology.proteinNADPH Oxidase 1Endothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressArteriosclerosis, thrombosis, and vascular biology
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