Atherosclerosis and its complications remain the major cause of death in the industrialized world and emerging economies worldwide. Dyslipidemia constitutes a major risk factor for the development and progression of atherosclerotic lesions, but may also lead to systemic disturbances - particularly metabolic dysfunction - that also influence cellular metabolism and function. Atherosclerotic lesions formation is initiated after retention of cholesterol-rich lipoproteins within the arterial wall at sites characterized by low shear stress. Modification of retained lipoproteins and activation of endothelial and vascular smooth muscle cells trigger an inflammatory response and provoke a series of cellular events involving complex interactions between vascular cells, innate immune cells (e.g., neutrophils, monocytes/macrophages, dendritic cells, mast cells, B1 B lymphocytes, innate lymphoid cells) and cells involved in adaptive immunity to atherosclerosis-related antigens (e.g., Th1, Tregs, B2 lymphocytes). Depending on the balance between pro-inflammatory responses and resolution promoting pathways, lesion development is either delayed or accelerated towards the formation of advanced and complex plaques characterized by chronic unresolved inflammation, extensive matrix remodelling and formation of large thrombogenic necrotic cores. Defective repair and weakening of the protective fibrous cap ultimately leads to plaque disruption, which triggers acute thrombosis and vascular occlusion.
The goal of this meeting is to provide attendees with a comprehensive overview of current research on atherosclerosis with a focus on the latest and most exciting developments in the immuno-metabolic mechanisms that govern disease initiation and progression. There is little doubt that the next most exciting therapy to combat cardiovascular disease will be based on targeting biological pathways that will have been discussed during this conference.
Seven sessions are planned and will highlight the following major research areas:
- vessel wall and endothelial cell biology
- lipids and modified lipids in inflammation
- cellular lipid metabolism and immunity
- lipoproteins and immune regulation
- extracellular vesicles
- innate immunity and metabolic regulation of innate immune functions
- epigenetics and regulation of gene expression in immune cells
- mechanisms involving inflammasome activation of monocyte/macrophages
- trained immunity, pro- and anti-atherogenic mechanisms operated by selective subsets of T and B lymphocytes
- immunometabolism and lymphocytes
- aging and senescence in inflammation, hematopoiesis, and cardiovascular disease
- non coding RNAs in lipid metabolism and inflammation
- existing and validated targets that are now in late-phase clinical trials.
This conference will bring together a restricted but high-level group of scientists from different disciplines and participants from all career levels enabling thorough discussions of the latest research between established and young investigators and trainees, and cross-fertilization among scientists from a variety of backgrounds.
Ziad Mallat, Christoph Binder, and Eicke Latz (Co-Chairs) look forward to welcoming you to the Melia Nassau Beach, Nassau, The Bahamas, from March 1-4, 2020.
- Vessel wall and endothelial cells
- Lipids and extracellular vesicles
- Innate immunity and inflammasome
- Adaptive immunity
- Aging and senescence
- Genetics and gene regulation
Take advantage of this fantastic opportunity for students! Register an academic at the earlybird rate of $1,835 and bring a student for only $850. Unfortunately, Postdocs are not eligible. Both registration packages include; accommodation for the 01, 02, 03 March 2020 (on a shared basis for students) and a 24hour all-inclusive food and beverage package for the conference period. Academic registrations must be completed by 03 January 2020. Once registered, please contact Chloe Trundle to obtain a special registration link for your student.
Nicolas Bazan (LSU Health New Orleans)
Peter Carmeliet (VIB)
Navdeep Chandel (Northwestern University)
Vishwa Deep Dixit (Yale School of Medicine)
Benjamin Ebert (Harvard Stem Cell Insitiute)
Zahi Fayad (Icahn School of Medicine at Mount Sinai)
Carlos Fernandez-Hernando (Yale School of Medicine)
Chris Glass (University of California, San Diego)
Catherine Hedrick (La Jolla Institute for Immunology)
Claudia Kemper (National Heart, Lung, and Blood Institute)
Klaus Ley (La Jolla Institute for Immunology)
Musa Mhlanga (University of Cape Town)
Kathryn Moore (NYU School of Medicine)
Mihai Netea (Radboud University)
Luke O'Neill (Trinity College Dublin)
Gwendalyn Randolph (Washington University in St. Louis)
William Sessa (Yale School of Medicine)
Filip Swirski (MGH Harvard)
Alan Tall (Columbia University)
Clotilde Théry (Institut Curie)
Jan van Deursen (Mayo Clinic)
Cornelia Weyand (Stanford University)
We encourage young scientists/clinicians to attend and expect broad representation from various disciplines. The conference will especially appeal to scientists, scientists/clinicians in academia, biotech and pharmaceutical companies with interest in Cardiovascular Medicine/Biology, Immunology, Metabolic Diseases, Immuno-Metabolism, Molecular/Cellular Biology and Epigenetics.
Graduate students, postdocs and junior researchers will gain a cutting-edge overview of the field and will have the extraordinary opportunity to discuss the latest developments with world-leading experts in an informal and highly conducive setting.
At the conclusion of the meeting, the participants should be able to:
1. Describe and discuss the most research advances in our understanding of the origin and fate of innate and adaptive immune cells (macrophages, lymphocytes, lymphoid cells) and their critical functions in atherosclerosis.
2. Describe and discuss the basic molecular mechanisms that integrate cellular metabolism and the immune response in the context of dyslipidemia, obesity and atherosclerosis.
3. Describe and discuss novel research on the effects of aging and senescence and their pathophysiologic and therapeutic implications.
4. Discuss novel evidence-based opportunities to prevent and treat the immuno-metabolic disturbances of atherosclerosis.