Project: Autophagy in inflammation and inflammatory disorders (ATLANTIS), from basic insights to experimental therapy
2021-01-01 – 2024-12-31
- Abstract
Autophagy is crucial in the (patho)physiology, including inflammation, infection and cancer. Autophagy functions as a survival mechanism by maintaining viability during periods of stress, and by removing damaged organelles and toxic metabolites, such as protein aggregates or intracellular pathogens. The Atlantis research consortium (AuTophagy in InfLAmmatioN and inflammaTory dISorders) brings together a team of expert investigators from the complementary fields of autophagy, (cancer) cell death signaling, inflammation signaling, angiogenesis and atherosclerosis, and drug screening and medicinal chemistry. We will study in an integrated way the impact of autophagy and its pharmacological modulation in various vascular diseases with a focus on the endothelium and its functional interaction with immune cells in sepsis, tumor-driven (lymph)angiogenesis, and atherosclerosis.
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Development and validation of a high-throughput screening pipeline of compound libraries to target EMT
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- Journal Article
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- open access
RIPK1 ablation in T cells results in spontaneous enteropathy and TNF-driven villus atrophy
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- Journal Article
- A1
- open access
Macrophage caspase-8 inhibition accelerates necrotic core expansion in atheroma plaque in mice
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- Journal Article
- A1
- open access
Enhancing anti-tumor immunity through intratumoral combination therapy with amphiphilic conjugates of oxaliplatin and imidazoquinoline TLR7/8 agonist
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- Journal Article
- A1
- open access
Detection of chimeric alpha-defensin transcripts and peptides in mouse Paneth cells
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- Journal Article
- A1
- open access
Harnessing luciferase chemistry in regulated cell death modalities and autophagy : overview and perspectives
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- Journal Article
- A1
- open access
The thymus road to a T cell : migration, selection, and atrophy
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- Journal Article
- A1
- open access
Metabolite-based inter-kingdom communication controls intestinal tissue recovery following chemotherapeutic injury
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- Journal Article
- A1
- open access
RIPK1 is dispensable for cell death regulation in β-cells during hyperglycemia
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- Journal Article
- A1
- open access
Ferroptosis in health and disease