A5089978523- Autophagy in Disease and Therapy
- Atherosclerosis and Cardiovascular Diseases
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Telomeres, Telomerase, and Senescence
- Sirtuins and Resveratrol in Medicine
- Adipokines, Inflammation, and Metabolic Diseases
- Advanced Glycation End Products research
- Phagocytosis and Immune Regulation
- Calpain Protease Function and Regulation
- Cardiovascular Function and Risk Factors
- Cell Adhesion Molecules Research
- Adipose Tissue and Metabolism
- PARP inhibition in cancer therapy
- Neuroinflammation and Neurodegeneration Mechanisms
- Tea Polyphenols and Effects
- Inflammasome and immune disorders
- Cardiac Fibrosis and Remodeling
- Cell death mechanisms and regulation
- Galectins and Cancer Biology
- Hippo pathway signaling and YAP/TAZ
- Electron Spin Resonance Studies
- Apelin-related biomedical research
- Immune cells in cancer
- Caveolin-1 and cellular processes
- Medical and Biological Ozone Research
UCLouvain
2024-2025
KU Leuven
2023-2025
Addenbrooke's Hospital
2018-2022
University of Cambridge
2018-2022
University of Antwerp
2015-2021
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...
Rationale: Vascular smooth muscle cell (VSMC) senescence promotes atherosclerosis and features of plaque instability, in part, through lipid-mediated oxidative DNA damage telomere dysfunction. SIRT6 (Sirtuin 6) is a nuclear deacetylase involved response signaling, inflammation, metabolism; however, its role regulating VSMC unclear. Objective: We examined expression human VSMCs, the role, regulation, downstream pathways activated by SIRT6, how regulates atherogenesis. Methods Results:...
Accumulation of vascular smooth muscle cells (VSMCs) is a hallmark multiple pathologies, including following neointimal formation after injury and atherosclerosis. However, human VSMCs in advanced atherosclerotic lesions show reduced cell proliferation, extensive persistent DNA damage, features premature senescence. Here, we report that stress-induced senescence (SIPS) stable expression telomeric repeat-binding factor 2 protein mutant (TRF2T188A) induce VSMCs, associated with damage. VSMC...
Abstract Aims Microvascular dysfunction has been proposed to drive heart failure with preserved ejection fraction (HFpEF), but the initiating molecular and cellular events are largely unknown. Our objective was determine when microvascular alterations in HFpEF begin, how they contribute disease progression, pericyte plays a role herein. Methods results dysfunction, characterized by inflammatory activation, loss of junctional barrier function, altered pericyte–endothelial crosstalk, assessed...
Heart failure with preserved ejection fraction (HFpEF) is a complex cardiovascular disease associated metabolic comorbidities. Microvascular dysfunction has been proposed to drive HFpEF, likely via endothelial cell (EC) dysfunction, yet the role of mural cells herein never explored. We used diabetic db/db mouse given 1% salt as new model HFpEF and crossed then PDGFRβtg/tg-CreERT2-EYFPtg/tg mice label cells. combined single-cell RNA sequencing, NichetNet analysis histology determine in HFpEF....
Apoptosis of macrophages and vascular smooth muscle cells (VSMCs) in advanced atherosclerotic plaques contributes to plaque progression instability. Caspase‐3, a key executioner protease the apoptotic pathway, has been identified human mouse but its role atherogenesis is not fully explored. We therefore investigated impact caspase‐3 deletion on atherosclerosis by crossbreeding knockout (Casp3 −/− ) mice with apolipoprotein E (ApoE mice. Bone marrow‐derived VSMCs isolated from Casp3 ApoE were...
Background and aims Increased evidence suggests a pro-atherogenic role for conventional dendritic cells (cDC). However, due to the lack of an exclusive marker cDC, their exact contribution atherosclerosis remains elusive. Recently, unique transcription factor was described namely Zbtb46, enabling us selectively target this cell type in mice. Methods Low-density lipoprotein receptor-deficient (Ldlr-/-) mice were transplanted with bone marrow from Zbtb46-diphtheria toxin receptor (DTR)...
Abstract Background Coronary microvascular dysfunction (CMD) participates in the pathophysiology of multiple cardiovascular diseases, but treatment options are limited. A new option may include ERBB4 stimulation by neuregulin-1 (NRG1), which has anti-inflammatory, antifibrotic, and cardioprotective effects models heart failure. Objectives To assess effect NRG1/ERBB4 on CMD hypertensive disease. Methods Hypertensive disease was induced 12 Aachener minipigs implantation deoxycorticosterone...
<h3>Aim</h3> Vascular smooth muscle cells (VSMCs) accumulate in injury-induced neointimal lesions and atherosclerotic plaques an oligoclonal fashion, yet plaque VSMCs show reduced proliferation cell senescence. DNA damage leads to VSMC senescence inflammation, promotes atherosclerosis; however, the exact mechanism by which lesion formation is not known. Here, we investigated telomere damage-induced senescence, contribution of senescence-induced inflammation mechanisms involved, consequences...