A5059965685- Phagocytosis and Immune Regulation
- Autophagy in Disease and Therapy
- Atherosclerosis and Cardiovascular Diseases
- Lung Cancer Treatments and Mutations
- Cancer Treatment and Pharmacology
- Immune cells in cancer
- Cell death mechanisms and regulation
- Chemotherapy-induced organ toxicity mitigation
- Lung Cancer Research Studies
- Prostate Cancer Treatment and Research
- Immunotherapy and Immune Responses
- Head and Neck Cancer Studies
- Cancer Immunotherapy and Biomarkers
- Lipoproteins and Cardiovascular Health
- Chemotherapy-related skin toxicity
- Nitric Oxide and Endothelin Effects
- Palliative Care and End-of-Life Issues
- Extracellular vesicles in disease
- Adipokines, Inflammation, and Metabolic Diseases
- Cell Adhesion Molecules Research
- Frailty in Older Adults
- Childhood Cancer Survivors' Quality of Life
- Neuroendocrine Tumor Research Advances
- Cardiovascular Health and Disease Prevention
- Peptidase Inhibition and Analysis
University of Antwerp
2012-2023
Universitair Ziekenhuis Leuven
1998-2021
KU Leuven
2014-2021
Ziekenhuisnetwerk Antwerpen Stuivenberg
2004-2019
ZNA Middelheim Hospital
1997-2018
HistoGeneX (Belgium)
2002-2018
Fund for Scientific Research
2015
Columbia University
2008-2009
Antwerp University Hospital
1994-2007
European Society for Medical Oncology
2003
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)...
Objective— Atherosclerotic plaques that are prone to disruption and acute thrombotic vascular events characterized by large necrotic cores. Necrotic cores result from the combination of macrophage apoptosis defective phagocytic clearance (efferocytosis) these apoptotic cells. We previously showed macrophages with tyrosine kinase-defective Mertk receptor (Mertk KD ) have a defect in vitro. Herein we test hypothesis mutation would increased accumulation cells promote core expansion mouse model...
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...
Anaemia and iron deficiency (ID) are frequent complications in patients with solid tumours or haematological malignancies, particularly treated chemotherapeutic agents [1.Ludwig H. Van Belle S. Barrett-Lee P. The European Cancer Survey (ECAS): a large, multinational, prospective survey defining the prevalence, incidence, treatment of anaemia cancer patients.Eur J Cancer. 2004; 40: 2293-2306http://dx.doi.org/10.1016/j.ejca.2004.06.019Abstract Full Text PDF PubMed Scopus (614) Google Scholar,...
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...
ER stress occurs in macrophage-rich areas of advanced atherosclerotic lesions and contributes to macrophage apoptosis subsequent plaque necrosis. Therefore, signaling pathways that alter stress–induced may affect atherosclerosis. Here we placed Apoe–/– mice deficient p38α MAPK on a Western diet found they had marked increase The p38α–deficient also exhibited significant reduction collagen content thinning the fibrous cap, which suggests progression was these mice. Consistent with our vivo...
Advanced care planning (ACP) is a process of reflection and communication about person's values wishes concerning future health issues personal preferences in the event that one becomes incapable consenting to or refusing treatment other [1.Definition advance http://www.advancecareplanning.ca/about-advance-care-planning.aspx (18 July 2014, date last accessed).Google Scholar]. It based on priorities, beliefs involves taking time learn end-of-life options services before crisis occurs. When...
The neuregulin-1 (NRG-1)/receptor tyrosine-protein kinase erbB (ErbB) system is an endothelium-controlled paracrine modulating cardiac performance and adaptation. Recent studies have indicated that NRG-1 has antifibrotic effects in the left ventricle, which were explained by direct actions on fibroblasts. However, NRG-1/ErbB also regulates function of macrophages. In this study, we hypothesized effect heart at least partially mediated through inhibitory We may be active other organs, such as...
In the last decades, search for mechanisms underlying progressive arterial stiffening and interventions to avoid or reverse this process has gained much attention. general, displays regional variation is, example, during aging more prominent in elastic than muscular arteries. We hypothesize that besides passive also active regulators of compliance [i.e., endothelial vascular smooth muscle cell (VSMC) function] differ between these Hence, it is conceivable vessel types will display different...
Oxysterols such as 7-ketocholesterol (7-KC) are important mediators of cell death in atherosclerosis. Therefore, vitro studies human smooth muscle (SMC) response to 7-KC were undertaken investigate the potential mechanisms.Human aortic SMCs treated with showed enhanced immunoreactivity for oxidative stress marker 4-hydroxy-2-nonenal and upregulated several genes (70-kDa heat shock protein 1, heme oxygenase growth arrest DNA damage-inducible 153) at mRNA but not level. 7-KC-treated rapidly...
Background and purpose: 7‐Ketocholesterol, an oxysterol present in atherosclerotic lesions, induces smooth muscle cell (SMC) death, thereby destabilizing plaques. Statins protect patients from myocardial infarction, though they induce SMC apoptosis. We investigated whether statins 7‐ketocholesterol exerted additive death effects. Experimental approach: Cultured rabbit aorta SMCs (passage 2–6) were exposed to with or without fluvastatin, simvastatin pravastatin. Uptake of neutral red (NR),...