A5060503236- Lipoproteins and Cardiovascular Health
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Cancer, Lipids, and Metabolism
- Cardiovascular Function and Risk Factors
- Health Systems, Economic Evaluations, Quality of Life
- Atrial Fibrillation Management and Outcomes
- Heart Failure Treatment and Management
- Atherosclerosis and Cardiovascular Diseases
- Blood Pressure and Hypertension Studies
- Cholesterol and Lipid Metabolism
- Heart Rate Variability and Autonomic Control
- Cardiac Imaging and Diagnostics
- Antiplatelet Therapy and Cardiovascular Diseases
- Pharmaceutical Economics and Policy
- Acute Ischemic Stroke Management
- Heart rate and cardiovascular health
- Medication Adherence and Compliance
- Cardiovascular Effects of Exercise
- Cardiac Valve Diseases and Treatments
- Lipid metabolism and disorders
- Diabetes Treatment and Management
- Nitric Oxide and Endothelin Effects
- Angiogenesis and VEGF in Cancer
- Hormonal Regulation and Hypertension
- Cardiac electrophysiology and arrhythmias
Klinik und Poliklinik für Neurologie
2011-2025
University Hospital Leipzig
2017-2025
Leipzig University
2018-2025
GTx (United States)
2024
Klinik und Poliklinik für Hals-, Nasen-, Ohrenheilkunde
2024
Universitätsklinikum des Saarlandes
2012-2023
Leipzig Heart Institute
2023
National Medical Research Center of Cardiology
2023
Institute of Experimental Cardiology
2023
Research Institute of Human Morphology
2023
Oxidized low-density lipoprotein (ox-LDL) causes endothelial dysfunction in part by decreasing the availability of nitric oxide (NO). Although HMG CoA reductase inhibitors restore function reducing serum cholesterol levels, it is not known whether they can also directly upregulate NO synthase (ecNOS) activity.Human saphenous vein cells were treated with ox-LDL (50 microg/mL thiobarbituric acid reactive substances 12 to 16 nmol/mg) presence simvastatin and lovastatin. In a time-dependent...
Abstract
The mechanism by which 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors increase endothelial nitric oxide synthase (eNOS) expression is unknown. To determine whether changes in isoprenoid synthesis affects eNOS expression, human cells were treated with the HMG-CoA inhibitor, mevastatin (1–10 μm), presence ofl-mevalonate (200 geranylgeranylpyrophosphate (GGPP, 1–10 farnesylpyrophosphate (FPP, 5–10 or low density lipoprotein (LDL, 1 mg/ml). Mevastatin increased mRNA and protein levels...
The treatment of ischemic strokes is limited to prophylactic agents that block the coagulation cascade. Here, we show cholesterol-lowering agents, 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, protect against cerebral injury by a previously unidentified mechanism involving selective up-regulation endothelial NO synthase (eNOS). Prophylactic with HMG-CoA inhibitors augments blood flow, reduces infarct size, and improves neurological function in normocholesterolemic mice. eNOS not...
Background— The molecular mechanisms by which physical training improves peripheral and coronary artery disease are poorly understood. Bone marrow–derived endothelial progenitor cells (EPCs) thought to exert beneficial effects on atherosclerosis, angiogenesis, vascular repair. Methods Results— To study the effect of activity bone marrow, EPCs were quantified fluorescence-activated cell sorter analysis in mice randomized running wheels (5.1±0.8 km/d, n=12 16 per group) or no wheel. Numbers...
Endothelial cell damage is one important pathophysiological step of atherosclerosis and restenosis after angioplasty. Accelerated reendothelialization impairs neointima formation. We evaluated the role intravenously transfused endothelial progenitor cells (EPCs) on formation in a mouse model arterial injury. Spleen-derived mononuclear (MNCs) were cultured basal medium. A total 91.8+/-3.2% adherent showed uptake acetylated low-density lipoprotein (Dil-Ac-LDL) lectin binding 4 days....
3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) may exert direct effects on vascular cells and beneficially influence endothelial dysfunction. Because reactive oxygen species (ROS) lead to damage dysfunction, we investigated the effect of atorvastatin ROS production underlying mechanisms in vitro vivo. Cultured rat aortic smooth muscle were incubated with 10 μmol/L atorvastatin. Angiotensin II–induced epidermal growth factor–induced significantly reduced by...
<h3>Importance</h3> Triglycerides and cholesterol are both carried in plasma by apolipoprotein B (ApoB)–containing lipoprotein particles. It is unknown whether lowering triglyceride levels reduces the risk of cardiovascular events to same extent as low-density (LDL-C) levels. <h3>Objective</h3> To compare association triglyceride-lowering variants lipase (<i>LPL</i>) gene LDL-C–lowering LDL receptor (<i>LDLR</i>) with disease per unit change ApoB. <h3>Design, Setting, Participants</h3>...
HMG-CoA Reductase Inhibitors (statins) reduce cardiac event rates in patients with stable coronary heart disease. Withdrawal of chronic statin treatment during acute syndromes may impair vascular function independent lipid-lowering effects and thus increase rate. We investigated the statins on rate 1616 Platelet Receptor Inhibition Ischemic Syndrome Management (PRISM) study who had artery disease chest pain previous 24 hours. recorded death nonfatal myocardial infarction 30-day follow-up....
Abstract —3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) significantly reduce cardiovascular mortality associated with hypercholesterolemia. There is evidence that statins exert beneficial effects in part through direct on vascular cells independent of lowering plasma cholesterol. We characterized the effect a 30-day treatment atorvastatin normocholesterolemic, spontaneously hypertensive rats (SHR). Systolic blood pressure was decreased atorvastatin-treated...
Atherosclerosis and restenosis after vascular injury are both characterized by endothelial dysfunction, apoptosis, inappropriate endothelialization, neointimal formation. Bone marrow-derived progenitor cells have been implicated in neovascularization, resulting adult blood vessel Despite the anticipated stem cell plasticity, role of bone has not clarified lesion development.We investigated formation mice transplantation marrow transfected means retrovirus with enhanced green fluorescent...
Reactive oxygen species (ROS) contribute to the development of heart failure. A potential source myocardial ROS is NADPH oxidase, which regulated by small GTP-binding protein rac1. Isoprenylation rac1 can be inhibited statin therapy. Thus, we examined and in human failing myocardium tested their regulation statins vivo.In left ventricular from patients with ischemic cardiomyopathy (ICM) or dilated (DCM), oxidase activity was increased 1.5-fold compared nonfailing controls (P<0.05, n=8). In...
Hypoxia induces vasoconstriction, in part, by down-regulating endothelial cell nitric oxide synthase (ecNOS) expression. Previous studies indicate that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase inhibitors improve endothelium-dependent relaxation increasing ecNOS activity. To determine whether HMG CoA can prevent hypoxia-mediated down-regulation of function and expression, human cells were exposed to hypoxia (3% O2) the presence simvastatin lovastatin for various durations...
The mechanism by which platelet-derived growth factor (PDGF) regulates vascular smooth muscle cell (SMC) DNA synthesis is unknown, but may involve isoprenoid intermediates of the cholesterol biosynthetic pathway. Inhibition with 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, simvastatin (Sim, 1–10 μm), inhibited PDGF-induced SMC >95%, retinoblastoma gene product hyperphosphorylation 90%, and cyclin-dependent kinases (cdk)-2, -4, -6 activity 80 ± 5, 50 3, 48 3%, respectively. This...
Background— The underlying molecular mechanisms of the vasculoprotective effects physical exercise are incompletely understood. Telomere erosion is a central component aging, and telomere-associated proteins regulate cellular senescence survival. This study examines exercising on vascular telomere biology endothelial apoptosis in mice long-term endurance training humans. Methods Results— C57/Bl6 were randomized to voluntary running or no wheel conditions for 3 weeks. Exercise upregulated...
Background Inability to tolerate statins because of muscle symptoms contributes uncontrolled cholesterol levels and insufficient cardiovascular risk reduction. Bempedoic acid, a prodrug that is activated by hepatic enzyme not present in skeletal muscle, inhibits ATP ‐citrate lyase, an upstream β‐hydroxy β‐methylglutaryl‐coenzyme A reductase the biosynthesis pathway. Methods Results The phase 3, double‐blind, placebo‐controlled CLEAR (Cholesterol Lowering via ACL‐Inhibiting Regimen) Serenity...
Due to the SARS-CoV2 pandemic, medical face masks are widely recommended for a large number of individuals and long durations. The effect wearing surgical FFP2/N95 mask on cardiopulmonary exercise capacity has not been systematically reported.This prospective cross-over study quantitated effects no (nm), (sm) (ffpm) in 12 healthy males (age 38.1 ± 6.2 years, BMI 24.5 2.0 kg/m2). 36 tests were performed randomized order. metabolic responses monitored by ergo-spirometry impedance cardiography....