A5082760959- Atherosclerosis and Cardiovascular Diseases
- Chemokine receptors and signaling
- Single-cell and spatial transcriptomics
- Immune cells in cancer
- T-cell and B-cell Immunology
- Cell Adhesion Molecules Research
- Adipokines, Inflammation, and Metabolic Diseases
- Phagocytosis and Immune Regulation
- Circadian rhythm and melatonin
- Cancer Immunotherapy and Biomarkers
- Cardiac Ischemia and Reperfusion
- Cancer Research and Treatments
- Epigenetics and DNA Methylation
- Blood disorders and treatments
- Erythrocyte Function and Pathophysiology
- interferon and immune responses
- Biomarkers in Disease Mechanisms
- Adenosine and Purinergic Signaling
- Receptor Mechanisms and Signaling
- Virus-based gene therapy research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cytokine Signaling Pathways and Interactions
- Renin-Angiotensin System Studies
- Immune Response and Inflammation
- Cardiac Fibrosis and Remodeling
Ludwig-Maximilians-Universität München
2016-2025
Mayo Clinic in Arizona
2025
Mayo Clinic
2024
Institute for Sports Medicine
2024
German Centre for Cardiovascular Research
2017-2022
Maastricht University
2017
Karolinska Institutet
2017
Max Delbrück Center
2016-2017
Deutsches Herzzentrum München
2017
Research Article25 May 2016Open Access Transparent process The time-of-day of myocardial infarction onset affects healing through oscillations in cardiac neutrophil recruitment Maximilian J Schloss Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU) Munich, Germany Search more papers by this author Michael Horckmans Katrin Nitz Max Delbrueck Center Molecular Medicine the Helmholtz Association, Berlin, Johan Duchene Maik Drechsler German Centre (DZHK), partner...
Abstract Atherosclerosis is a major underlying cause of cardiovascular disease. Previous studies showed that inhibition the co-stimulatory CD40 ligand (CD40L)-CD40 signaling axis profoundly attenuates atherosclerosis. As CD40L exerts multiple functions depending on cell-cell interactions involved, we sought to investigate function most relevant CD40L-expressing cell types in atherosclerosis: T cells and platelets. Atherosclerosis-prone mice with CD40L-deficiency CD4 + display impaired Th1...
Abstract CCL17 is produced by conventional dendritic cells, signals through CCR4 on regulatory T (T reg ) cells and drives atherosclerosis suppressing functions yet undefined mechanisms. Here we show that from CCL17-deficient mice display a pro-tolerogenic phenotype transcriptome not phenocopied in lacking its cognate receptor CCR4. In the plasma of mice, CCL3 was only decreased cytokine/chemokine. We found signaled CCR8 as an alternate high-affinity receptor, which induced expression...
Amino acid metabolism is crucial for inflammatory processes during atherogenesis. The endogenous amino homoarginine a robust biomarker cardiovascular outcome and mortality with high levels being protective. However, the underlying mechanisms remain elusive. We investigated effect of supplementation on atherosclerotic plaque development particular focus inflammation.Female ApoE-deficient mice were supplemented (14 mg/L) in drinking water starting 2 weeks before continuing throughout 6-week...
BACKGROUND: The activation and polarization of T cells play a crucial role in atherosclerosis dictate athero-inflammation. epigenetic enzyme EZH2 (enhancer zeste homolog 2) mediates the H3K27me3 (trimethylation histone H3 lysine 27) is pivotal controlling cell responses. METHODS: To detail atherosclerosis, we used human carotid endarterectomy specimens to reveal plaque expression geography EZH2. Atherosclerosis-prone Apoe (apolipoprotein E)–deficient mice with CD (cluster differentiation) 4...
Abstract Aims GITR—a co-stimulatory immune checkpoint protein—is known for both its activating and regulating effects on T-cells. As atherosclerosis bears features of chronic inflammation autoimmunity, we investigated the relevance GITR in cardiovascular disease (CVD). Methods results expression was elevated carotid endarterectomy specimens obtained from patients with cerebrovascular events (n = 100) compared to asymptomatic 93) correlated parameters plaque vulnerability, including...
Objective— Circadian regulation of neutrophil homeostasis affects myocardial infarction (MI) healing. It is unknown whether diurnal variations monocyte counts exist in the heart and this their cardiac infiltration response to MI. Approach Results— Murine blood organs were harvested at distinct times day analyzed by flow cytometry. Ly6C high surface expression levels chemokine receptors (CCR) ≈2-fold higher beginning active phase, Zeitgeber Time (ZT) 13 compared with ZT5. This was because...
Introduction Atherosclerosis is a lipid-driven inflammatory disease of the arterial wall, and underlying cause majority cardiovascular diseases. Recent advances in high-parametric immunophenotyping immune cells indicate that T constitute major leukocyte population atherosclerotic plaque. The E3 ubiquitin ligase Casitas B-lymphoma proto-oncogene-B (CBL-B) critical intracellular regulator sets threshold for cell activation, making CBL-B potential therapeutic target to modulate inflammation...
Abstract Background Atherosclerosis is a chronic inflammatory disease and the primary underlying cause of cardiovascular (CVD). Recently, intracellular metabolic pathways have been identified as master switches immune cell function thus seem promising targets for therapeutic interventions aimed at lowering inflammation thereby atherogenesis. Decades research demonstrated importance amino acid (AA) L-arginine (Arg) in CVD. Although most has focused on endothelium-dependent effects Arg by...
The CD40-CD40L co-stimulatory dyad has been identified as critical player in atherosclerosis. Our previous work shown that CD40 and CD40L have cell divergent effects on Deficiency of the dendritic cell-T axis decreased atherosclerosis via reducing T helper 1 responses, whereas deficiency macrophages reduced by enhancing efferocytosis necrotic core content. is highly expressed B cells interacts with to induce antibody production follicular responses. We therefore hypothesize deletion will...
Abstract Background Atherosclerosis is a chronic inflammatory disease, characterized by the formation of luminal plaques in arteries. Atheroprogression accompanied strong immune activation, during which T cells play pivotal role. Genes driving T-cell activation are regulated polycomb repressive complex 2(PRC2), whose major component Enhancer Zeste Homolog 2(EZH2), responsible for methylation Histone 3 Lysine 27(H3K27me3) epigenetic mark. Purpose We hypothesize that EZH2 mediates and...
Abstract Background The co-stimulatory CD40–CD40 ligand axis is central in atherogenesis. Upon activation, CD40 recruits tumor necrosis factor receptor-associated factors (TRAFs) to induce downstream signaling. Murine studies with mutated CD40-TRAF binding sites macrophages have shown that the CD40-TRAF6, rather than CD40-TRAF2/3/5, crucial for atherosclerosis. We thus synthesized small molecule inhibitor TRAF-STOP 6877002, selectively blocks CD40-TRAF6 6877002 successfully reduced onset and...
Abstract Background The trimethylation status of Histone 3 Lysine 27 (H3K27), which is regulated by the methylating enzyme Enchancer zeste homolog 2 (EZH2) and demethylating Jumonji domain containing (JMJD3), a critical epigenetic signature for differentiation polarization T cells. During atherogenesis, cells initiate propagate lesion formation through imbalanced helper (Th) leading to accumulation pro-atherogenic cell subsets, including Th1, that exacerbate inflammation. Purpose We...