A5059862918- Autophagy in Disease and Therapy
- Atherosclerosis and Cardiovascular Diseases
- Cardiovascular Health and Disease Prevention
- Nitric Oxide and Endothelin Effects
- Phagocytosis and Immune Regulation
- Cerebrovascular and Carotid Artery Diseases
- Angiogenesis and VEGF in Cancer
- Coronary Interventions and Diagnostics
- Neuroscience and Neuropharmacology Research
- Lipoproteins and Cardiovascular Health
- Cardiovascular Disease and Adiposity
- Cell death mechanisms and regulation
- Protease and Inhibitor Mechanisms
- Cell Adhesion Molecules Research
- Cardiovascular Function and Risk Factors
- Religion, Theology, and Education
- Adipokines, Inflammation, and Metabolic Diseases
- Receptor Mechanisms and Signaling
- Pharmaceutical Practices and Patient Outcomes
- Cancer, Lipids, and Metabolism
- Adipose Tissue and Metabolism
- Cellular transport and secretion
- Extracellular vesicles in disease
- Health Systems, Economic Evaluations, Quality of Life
- Calpain Protease Function and Regulation
University of Antwerp
2016-2025
RWTH Aachen University
2010-2022
Antwerp University Hospital
1997-2017
iMinds
2015
École Polytechnique Fédérale de Lausanne
2015
Ghent University
2015
ZNA Middelheim Hospital
1994-2012
Laboratoire de Chimie
2012
Max Planck Society
1994-2010
Max Planck Institute of Experimental Medicine
2003-2009
Apoptotic cell death has been demonstrated in advanced human atherosclerotic plaques. cells (ACs) should be rapidly removed by macrophages, otherwise secondary necrosis occurs, which turn elicits inflammatory responses and plaque progression. Therefore, we investigated the efficiency of phagocytosis ACs macrophages atherosclerosis.Human endarterectomy specimens tonsils were costained for CD68 (macrophages) terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)...
Background —The transition of a fatty streak into an atherosclerotic plaque is characterized by the appearance focal and diffuse regions cell death. We have investigated distribution apoptotic death apoptosis-related proteins in early advanced lesions. Methods Results —Human plaques were studied whole-mount carotid endarterectomy specimens (n=18). This approach allowed comparison adaptive intimal thickenings, streaks, same patient. The streaks differed from thickenings presence BAX ( P...
Background— The formation of reactive oxygen species is a critical event in atherosclerosis because it promotes cell proliferation, hypertrophy, growth arrest, and/or apoptosis and oxidation LDL. In the present study, we investigated whether species-induced oxidative damage to DNA occurs human atherosclerotic plaques this accompanied by upregulation repair mechanisms. Methods Results— We observed increased immunoreactivity against marker 7,8-dihydro-8-oxo-2′-deoxyguanosine (8-oxo-dG) carotid...
Autophagy is triggered in vascular smooth muscle cells (VSMCs) of diseased arterial vessels. However, the role VSMC autophagy cardiovascular disease poorly understood. Therefore, we investigated effect defective on survival and phenotype its significance development postinjury neointima formation atherosclerosis. Tissue-specific deletion essential gene Atg7 murine VSMCs (atg7−/− VSMCs) caused accumulation SQSTM1/p62 accelerated stress-induced premature senescence as shown by cellular nuclear...
Objective— Previously, we demonstrated that activated inducible NO synthase (iNOS)-expressing foam cells in human carotid plaques often produce autofluorescent (per)oxidized lipids (ceroid). Here, investigate whether intraplaque microvessels can provide with and trigger macrophage activation. Methods Results— Microvessels (von Willebrand factor [vWf] immunoreactivity), macrophages (iNOS ceroid were systematically mapped longitudinal sections of 15 endarterectomy specimens. An unbiased...
There is a need for animal models of plaque rupture. We previously reported that elastin fragmentation, due to mutation (C1039G+/−) in the fibrillin-1 (Fbn1) gene, promotes atherogenesis and highly unstable phenotype apolipoprotein E deficient (ApoE−/−) mice on Western-type diet (WD). Here, we investigated whether rupture occurred ApoE−/−Fbn1C1039G+/− was associated with myocardial infarction, stroke, sudden death. Female ApoE−/− were fed WD up 35 weeks. Compared mice, plaques showed...
Because of global aging, the prevalence heart failure with preserved ejection fraction (HFpEF) continues to rise. Although HFpEF pathophysiology remains incompletely understood, endothelial inflammation is stated play a central role. Cellular senescence process cellular growth arrest linked aging and inflammation. We used mice accelerated investigate role in development.Senescence-accelerated (SAM, n=18) control normal (n=15) were fed chow or high-fat, high-salt diet (WD). Vascular cardiac...