A5047426934- Signaling Pathways in Disease
- Adipokines, Inflammation, and Metabolic Diseases
- Cardiac Fibrosis and Remodeling
- Psoriasis: Treatment and Pathogenesis
- Atherosclerosis and Cardiovascular Diseases
- Inflammation biomarkers and pathways
- Asthma and respiratory diseases
- Neuroinflammation and Neurodegeneration Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Traumatic Brain Injury and Neurovascular Disturbances
- Nitric Oxide and Endothelin Effects
- Noise Effects and Management
- Photoacoustic and Ultrasonic Imaging
- Genomics and Phylogenetic Studies
- Dermatology and Skin Diseases
- Eicosanoids and Hypertension Pharmacology
- Polyamine Metabolism and Applications
- Heart Failure Treatment and Management
- Chemotherapy-induced cardiotoxicity and mitigation
- Ultrasound and Hyperthermia Applications
- Cytokine Signaling Pathways and Interactions
- Cholesterol and Lipid Metabolism
- Blood Coagulation and Thrombosis Mechanisms
- Genetics, Aging, and Longevity in Model Organisms
- Telomeres, Telomerase, and Senescence
Johannes Gutenberg University Mainz
2015-2025
University Medical Center of the Johannes Gutenberg University Mainz
2015-2025
German Centre for Cardiovascular Research
2019-2024
University Medical Center
2018
University of Illinois Urbana-Champaign
2014
University of Cambridge
1984-2013
Witten/Herdecke University
2013
University of Bonn
1993-1998
Queens University of Charlotte
1984
University Children's Hospital Tübingen
1983
Epidemiological studies have found that transportation noise increases the risk for cardiovascular morbidity and mortality, with solid evidence ischemic heart disease, failure, stroke. According to World Health Organization, at least 1.6 million healthy life years are lost annually from traffic-related in Western Europe. Traffic night causes fragmentation shortening of sleep, elevation stress hormone levels, increased oxidative vasculature brain. These factors can promote vascular...
Abstract Aims Mental stress substantially contributes to the initiation and progression of human disease, including cardiovascular conditions. We aim investigate underlying mechanisms these contributions since they remain largely unclear. Methods results Here, we show in humans mice that leucocytes deplete rapidly from blood after a single episode acute mental stress. Using cell-tracking experiments animal models stress, found exposure leads prompt uptake inflammatory distinct tissues heart,...
Atherosclerotic plaque development depends on chronic inflammation of the arterial wall. A dysbiotic gut microbiota can cause low-grade inflammation, and composition was linked to cardiovascular disease risk. However, role this environmental factor in atherothrombosis remains undefined. To analyze impact atherothrombosis, we rederived low-density lipoprotein receptor-deficient (Ldlr-/- ) mice as germfree (GF) kept these for 16 weeks an atherogenic high-fat Western diet (HFD) under GF...
Abstract Aim Recent evidence suggests that arterial hypertension could be alternatively explained as a physiological adaptation response to water shortage, termed aestivation, which relies on complex multi‐organ metabolic adjustments prevent dehydration. Here, we tested the hypothesis chronic loss across diseased skin leads similar adaptive conservation responses observed in experimental renal failure or high salt diet. Methods We studied mice with keratinocyte‐specific overexpression of...
Traffic noise may play an important role in the development and deterioration of ischaemic heart disease. Thus, we sought to determine mechanisms cardiovascular dysfunction inflammation induced by aircraft a mouse model myocardial infarction (MI) humans with incident MI.C57BL/6J mice were exposed alone (average sound pressure level 72 dB; peak 85 dB) for up 4 days, resulting pro-inflammatory aortic gene expression myeloid cell adhesion/diapedesis pathways. The promoted adhesion infiltration...
Abstract Aims Heart failure (HF) ensuing myocardial infarction (MI) is characterized by the initiation of a systemic inflammatory response. We aimed to elucidate impact myelomonocytic cells and their activation angiotensin II on vascular endothelial function in mouse model HF after MI. Methods results was induced male C57BL/6J mice permanent ligation left anterior descending coronary artery. Compared sham, had significantly impaired accompanied enhanced mobilization Sca-1+c-Kit+...
Despite major advances in acute interventions for myocardial infarction (MI), adverse cardiac remodeling and excess fibrosis after MI causing ischemic heart failure (IHF) remain a leading cause of death worldwide. Here we identify profibrotic coagulation signaling pathway that can be targeted improved function following with persistent ischemia. Quantitative phosphoproteomics tissue revealed an upregulated mitogen-activated protein kinase (MAPK) human IHF. Intervention this trametinib...
Heart failure (HF) coincides with cardiomyocyte telomere shortening. Arterial hypertension is the most prominent risk factor for HF. Both HF and arterial are associated dysregulation of neurohormonal axis. How activation linked to shortening in pathogenesis incompletely understood. Cardiomyocyte length was assessed a mouse model hypertensive induced by excess (AngII [angiotensin II] infusion, high salt diet, uninephrectomy), AngII-stimulated cardiomyocytes endomyocardial biopsies from...
Cardiovascular disease is the leading cause of burden and death worldwide fueled by vascular inflammation. CD40L-CD40-TRAF signaling involved in progression atherosclerosis drives development coronary heart (CHD). The present study investigates whether CD40L-CD40-TRAF6 pathway with focus on immune cells adipocytes could be a therapeutic target arterial hypertension. Arterial hypertension was induced WT (C57BL6/J) cell-specific CD40(L) knockout mice (AdipoqCre x CD40 fl/fl, CD4Cre CD19Cre...
The neutrophil recruiting cytokine Interleukin-17A (IL-17A) is a key component in vascular dysfunction and arterial hypertension. Moreover, IL-17A has central role for the infiltration of myeloid cells into wall Angiotensin II-induced inflammation. intention our study was to analyze impact T cell-derived on hypertension, function, Chronic overexpression (CD4-IL-17Aind/+ mice) resulted elevated reactive oxygen species peripheral blood significant compared control mice. seen CD4-IL-17Aind/+...
A sulfite-reductase-type protein was purified from the hyperthermophilic crenarchaeote Pyrobaculum islandicum grown chemoorganoheterotrophically with thiosulfate as terminal electron acceptor. In common dissimilatory sulfite reductases has an alpha 2 beta structure and contains high-spin sirohaem, non-haem iron acid-labile sulfide. The oxidized exhibits absorption maxima at 280, 392, 578 710 nm shoulders 430 610 nm. isoelectric point of pH 8.4 sets apart all characterized thus far. genes for...
Myelomonocytic cells are critical in injury and healing post-myocardial infarction (MI). Mechanisms of regulation, however, incompletely understood. The aim the study was to elucidate role interferon gamma (IFN-γ) orchestrated inflammatory response a murine model MI.MI induced 8- 12-week-old male mice (C57BL/6 background) by permanent ligation left anterior descending (LAD) coronary artery. Lysozyme M (LysM)+ cell-depleted LysMiDTR transgenic displayed reduced influx...
The cytokine interleukin-6 (IL-6) plays a central role in the inflammation cascade as well cardiovascular disease progression. Since myeloid cells are primary source of IL-6 formation, we aimed to generate mouse model study cell-derived vascular disease.
Pulmonary embolism (PE) results from deep vein thrombosis (DVT) and can lead to chronic thromboembolic pulmonary hypertension (CTEPH) involving vascular dysfunction. Mechanisms are incompletely understood, in part due lack of mouse models. We induced PE C57BL/6 mice by intravenous injection thrombin (166 U/kg BW), confirmed a sudden bradycardia, bradypnea, an increase artery (PA) pressure observed high-frequency ultrasound. While symptoms resolved rapidly after single application, repeated...
Excess fibrotic remodeling causes cardiac dysfunction in ischemic heart disease, driven by MAP (mitogen-activated protein) kinase-dependent TGF-ß1 (transforming growth factor-ß1) activation coagulation signaling of myeloid cells. How coagulation-inflammatory circuits can be specifically targeted to achieve beneficial macrophage reprogramming after myocardial infarction (MI) is not completely understood.
Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function survival. We aimed to elucidate the impact early treatment with ACE inhibitor ramipril on hematopoietic response MI, as well chronic systemic vascular inflammation. Methods Results: In mouse model induced by permanent ligation anterior descending artery, immediate initiation (10 mg/k/d via drinking water) reduced cardiac...
Erythrocytes (red blood cells) participate in the control of vascular NO bioavailability. The purpose this study was to determine whether and how genetic deletion ARG1 (arginase-1) affects smooth muscle cell signaling, osteoblastic differentiation, atherosclerotic lesion calcification.Atherosclerosis-prone mice with conditional, erythrocyte-restricted (apoE-/- red cell.ARG1 knockout) were generated calcification studied using molecular imaging osteogenic activity agent OsteoSense, Alizarin...
Abstract Cerebral hypoperfusion is a key factor for determining the outcome after subarachnoid hemorrhage (SAH). A subset of SAH patients develop neurogenic stress cardiomyopathy (NSC), but it unclear to what extent cerebral influenced by cardiac dysfunction SAH. The aims this study were examine association between function and perfusion in murine model identify electrocardiographic echocardiographic signs indicative NSC. We quantified cortical laser SPECKLE contrast imaging, myocardial...
Abstract Aims Assessment of endothelial function in humans by measuring flow-mediated dilation (FMD) risk-stratifies individuals with established cardiovascular disease, whereas its predictive value is limited primary prevention. We therefore aimed to establish and evaluate novel markers FMD at the population level. Methods results In order identify targets that were negatively correlated investigate their contribution vascular function, we performed a genome-wide association study (GWAS)...
Doxorubicin (DOX) is an important drug for the treatment of various tumor entities. However, occurrence heart failure limits its application. This study investigated differential gene expression profiles in left and right ventricles DOX treated mice with either preserved or impaired myocardial function. We provide new mechanistic insights into pathophysiology DOX-induced have discovered pathways that counteract cardiotoxicity. used total 48 male applied a chronic low dose administration (5...
Background: Psoriasis is hallmarked by vascular dysfunction, arterial hypertension, and an increased risk for cardiovascular diseases. We have shown recently that skin-driven interleukin (IL)-17A expression promotes psoriasis-like disease in mice, this associated with inflammation, hypertension. As intensive risk-factor reduction recommended psoriasis patients, we aimed to elucidate the impact of angiotensin II receptor type 1 (AT1) antagonist telmisartan a mouse model severe skin disease....