A5044630700- Sirtuins and Resveratrol in Medicine
- Cardiac Ischemia and Reperfusion
- Adipose Tissue and Metabolism
- Adipokines, Inflammation, and Metabolic Diseases
- Adenosine and Purinergic Signaling
- Mitochondrial Function and Pathology
- Cardiovascular Disease and Adiposity
- Cardiac Fibrosis and Remodeling
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Calpain Protease Function and Regulation
- Neuroinflammation and Neurodegeneration Mechanisms
- Autophagy in Disease and Therapy
- Cardiovascular Function and Risk Factors
- Mechanical Circulatory Support Devices
- Signaling Pathways in Disease
- Biochemical effects in animals
- Pharmacological Receptor Mechanisms and Effects
- Glutathione Transferases and Polymorphisms
- Renin-Angiotensin System Studies
- Regulation of Appetite and Obesity
- RNA regulation and disease
- Transplantation: Methods and Outcomes
- Biosimilars and Bioanalytical Methods
- Viral Infections and Immunology Research
- Estrogen and related hormone effects
University of Freiburg
2015-2025
University Medical Center Freiburg
2011-2024
Universitäts-Herzzentrum Freiburg-Bad Krozingen
2017-2019
Christophorus Kliniken
2015
Background: Platelets store large amounts of serotonin that they release during thrombus formation or acute inflammation. This facilitates hemostasis and modulates the inflammatory response. Methods: Infarct size, heart function, cell composition were analyzed in mouse models myocardial reperfusion injury with genetic pharmacological depletion platelet serotonin. These studies complemented by vitro stimulation assays platelets leukocytes mice men, measuring plasma levels leukocyte activation...
How mitochondria reconcile roles in functionally divergent cell death pathways of apoptosis and NLRP3 inflammasome-mediated pyroptosis remains elusive, as is their precise role activation the evolutionarily conserved physiological function NLRP3. Here, we have shown that when cells were challenged simultaneously, was inhibited prevailed. Apoptosis inhibition by structurally diverse activators, including nigericin, imiquimod, extracellular ATP, particles, viruses, not a consequence...
Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a crucial role in cholesterol homeostasis by regulating low-density lipoprotein (LDL) receptor levels. Despite its known effects on metabolism, the of PCSK9 cardiac function, especially post-myocardial infarction (MI), remains unclear. This study investigates impact heart function post-MI evaluates inhibition via Alirocumab. Methods We used knockout (KO) mice wildtype (WT) vivo treatment with Alirocumab to...
Lack of the mitochondrial deacetylase sirtuin 3 (SIRT3) impairs function and increases susceptibility to induction permeability transition pore. Because these alterations contribute myocardial ischemia-reperfusion (IR) injury, we hypothesized that SIRT3 deficiency may increase cardiac injury following IR. Hearts 10-week-old mice were perfused in isolated working mode subjected 17.5 min global no-flow ischemia, followed by 30 reperfusion. Measurements before ischemia revealed a decrease power...
Abstract Glutathione‐ S ‐transferases (GSTs) are upregulated in malignant gliomas and contribute to their chemoresistance. The nitric oxide (NO) donor PABA/NO (O 2 ‐{2,4‐dinitro‐5‐[4‐( N ‐methylamino)benzoyloxy]phenyl} 1‐( , ‐dimethylamino)diazen‐1‐ium‐1,2‐diolate) generates NO upon selective enzymatic activation by GST‐π‐inducing biological effects tumors. Tumor cell killing chemosensitization were observed a variety of tumors after exposure GST‐activated drugs. In our project, cytotoxic...
MicroRNAs are key regulators of the cardiac response to injury. MiR-100 has recently been suggested be involved in different forms heart failure, but functional studies lacking. In present study, we examined impact transgenic miR-100 overexpression on structure and function during physiological aging pathological pressure-overload-induced failure mice after transverse aortic constriction surgery. was moderately upregulated induction pressure overload mice. While our model...
Impaired cardiac efficiency is a hallmark of diabetic cardiomyopathy in models type 2 diabetes. Adiponectin receptor 1 (AdipoR1) deficiency impairs non-diabetic mice, suggesting that hypoadiponectinemia diabetes may contribute to impaired due compromised AdipoR1 signaling. Thus, we investigated whether targeting adiponectin receptors improve function and energetics, attenuate mice.A non-selective agonist, AdipoRon, vehicle were injected intraperitoneally into Eight-week-old db/db or...
Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and exaggerated cardiac hypertrophy pressure overload, entities that are causally linked mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired function. Thus, it was our objective investigate whether impairs energetics the heart. At 8 weeks age, heart weight-to-body weight ratios were not different between knockout (ADQ-/-) mice wildtypes (WT). isolated working...
Objective: The accumulation of inflammatory leukocytes is a prerequisite adipose tissue inflammation during cardiometabolic disease. We previously reported that genetic deficiency the intracellular signaling adaptor TRAF5 (TNF [tumor necrosis factor] receptor–associated factor 5) accelerates atherosclerosis in mice by increasing cell recruitment. Here, we tested hypothesis an impairment modulates and its metabolic complications model diet-induced obesity mice. Approach Results: To induce...
Decreased serum adiponectin levels in type 2 diabetes has been linked to the onset of mitochondrial dysfunction diabetic complications by impairing AMPK-SIRT1-PGC-1α signaling via impaired receptor 1 (AdipoR1) signaling. Here, we aimed characterize previously undefined role disrupted AdipoR1 on protein composition cardiac, renal, and hepatic tissues as three organs principally associated with complications. Comparative proteomics were performed mitochondria isolated from heart, kidneys liver...
Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main source(s): CRC1425 - DFG Introduction Resident macrophages account for 5% the cells in healthy heart. In response to cardiac injury, monocytes infiltrate and differentiate into recruited complementing original resident macrophage population, together orchestrate remodeling. We aim identify extent which origin, tissue location type injury determine phenotypes ischemic non-ischemic injuries...
Abstract Sirtuin 4 (SIRT4) is a mitochondrial NAD+-dependent deacylase which inhibits the oxidation of glucose and fatty acids, has been implicated in regulation oxidative stress. Given importance cardiac energy depletion ROS during heart failure development, we aimed to define role SIRT4 development failure. Mice with deletion (SIRT4−/−) or overexpression (SIRT4 TG) were subjected transverse aortic constriction (TAC) for 12 weeks underwent sham procedures. Using echocardiography, ejection...
Introduction: Systemic inflammation and endothelial dysfunction have an important role for myocardial remodeling in heart failure with preserved ejection fraction (HFpEF).Microvascular leads to increased cardiomyocyte stiffness interstitial fibrosis which induce diastolic LV dysfunction.Nonetheless, optimal treatment remains widely undefined.Purpose: To examine whether exercise training would be able improve capacity, function, left ventricle (LV) exert antiinflammatory effect animal model...
Background: Myocardial reperfusion injury leads to platelet neutrophil complex (PNCs) migration into cardiac tissue, which promotes post-infarction necrosis. Local serotonin levels are elevated during ischemia and recruitment of inflammatory cells. Tryptophan hydroxylase-1-deficient mice (Tph1-/-) lack peripheral show attenuated response. We evaluated PNC infiltration after myocardial (I/R) in the absence serotonin. Methods: C57Bl/6 (WT) Tph1-/- underwent coronary artery ligation induce...
Sirtuin 3 (SIRT3) is a mitochondrial NAD+-dependent deacetylase which highly expressed in the heart, and increases ATP production. In failing hearts, reduced expression of SIRT3 associated with myocardial dysfunction. Thus, we hypothesized that may causally contribute to contractile dysfunction hearts. 24 week-old mice global knockout (SIRT3 KO), echocardiography revealed decreased ejection fraction (-10%), left ventricular posterior wall thickness (-11%) increased endsystolic volume (+26%;...