A5054279479- Climate Change and Health Impacts
- Eicosanoids and Hypertension Pharmacology
- Heme Oxygenase-1 and Carbon Monoxide
- Signaling Pathways in Disease
- Noise Effects and Management
- Immune cells in cancer
- Thermal Regulation in Medicine
- Renin-Angiotensin System Studies
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Mast cells and histamine
- Heart Failure Treatment and Management
- Cardiac Fibrosis and Remodeling
- Blood Coagulation and Thrombosis Mechanisms
- Biomarkers in Disease Mechanisms
- Hemophilia Treatment and Research
University Medical Center of the Johannes Gutenberg University Mainz
2022-2024
Johannes Gutenberg University Mainz
2022-2024
German Centre for Cardiovascular Research
2023
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...
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.
Abstract Background Excess fibrotic remodeling leads to cardiac dysfunction in ischemic heart disease and is driven by MAP kinase-dependent transforming growth factor-ß1 (TGF-ß1) activation coagulation signaling of myeloid cells. How coagulation-inflammatory circuits can be specifically targeted achieve beneficial macrophage reprogramming after myocardial infarction (MI) incompletely understood. Methods Mice with permanent ligation the proximal left anterior descending artery (LAD) were used...
Abstract Background Systemic arterial Hypertension is one of the most important risk factor responsible for morbidity and mortality world-wide. Angiotensin II (Ang II), a potent vasoconstrictor key player in renin-angiotensin-aldosterone system (RAAS) vascular dysfunction, inflammation, tissue damage. Heme oxygenase-1 (HO-1) overexpression may confer antioxidant anti-inflammatory properties Ang II-induced hypertension through its action on heme catabolism, generating carbon monoxide (CO),...
Abstract Background Increasing evidence suggests that FXI is an attractive target for antithrombotic therapy because it reduces thrombosis without increasing bleeding risk. Patients with decreased levels of are at reduced risk cardiovascular diseases and thromboembolic events. We have already revealed depletion inhibits the vascular coagulation-inflammatory circuit in angiotensin II-induced arterial hypertension. However, effect on cardiac inflammation function ischemia/reperfusion (I/R)...
Abstract Background Arterial hypertension is one of the most important modifiable risk factors for all-cause morbidity and mortality worldwide. Angiotensin II (Ang II) plays a pathogenic role in development hypertension, vascular dysfunction, inflammation tissue damage. In context heme-oxygenase 1 (HO-1) gene expression upregulated as an antioxidant defense system response to AngII through its action on heme catabolism, which generates carbon monoxide (CO), ferritin biliverdin, reduced...