Important Notice: Given the close proximity to the conference start date, hotel availability is likely to become very limited over the coming weeks. We are still currently able to accept registrations; however, this may change, so we would encourage prompt registration and payment to secure your accommodation. Once registration has been completed, please allow us up to 3 working days to confirm your hotel reservation with you. If there are any issues in accommodating, we will reach out promptly to discuss alternative options. A reminder: your hotel reservation is not secured until payment has been received in full.

Atherosclerosis and its complications remain the leading cause of death in industrialized nations and are rapidly emerging as a major health burden worldwide. Dyslipidemia is a central risk factor for the initiation and progression of atherosclerotic lesions. Beyond its direct vascular effects, it also contributes to local and systemic metabolic disturbances that alter cellular metabolism and function, thereby amplifying inflammatory responses and fueling disease progression.

Atherosclerotic lesion formation begins with the retention of cholesterol-rich lipoproteins in the arterial wall, particularly at sites exposed to low shear stress. Subsequent modification of these lipoproteins and activation of endothelial and vascular smooth muscle cells trigger an inflammatory cascade. This initiates a complex interplay among vascular cells, innate immune cells, and adaptive immune responses directed against atherosclerosis-related antigens. Recent studies have revealed remarkable heterogeneity within the immune cell compartment of atherosclerotic plaques. Depending on the balance between pro-inflammatory signals and pathways promoting resolution, lesion development may be slowed or accelerated, ultimately progressing to advanced plaques. These are characterized by persistent, unresolved inflammation, extensive extracellular matrix remodeling, and the formation of large thrombogenic necrotic cores resulting from impaired clearance of dying cells. Defective repair and weakening of the fibrous cap further predispose plaques to disruption, precipitating acute thrombosis and vascular occlusion.

Given this complexity, systems-level approaches are essential to unravel the mechanisms linking chronic inflammation with atherogenesis. Despite effective control of traditional cardiovascular risk factors, a substantial residual risk remains—largely attributable to inflammation. Yet, the precise triggers and sustaining mechanisms of vascular inflammation, the protective resilience factors, and the optimal strategies to therapeutically target these pathways remain incompletely understood.

Now in its fifth edition, this meeting is designed to provide participants with a comprehensive overview of cutting-edge research in atherosclerosis, with a particular emphasis on the latest discoveries in immuno-metabolic mechanisms driving disease initiation and progression. Therapies directly targeting immuno-inflammatory pathways in atherosclerotic cardiovascular disease are now closer to clinical application than ever before, underscoring the growing importance of translational perspectives. Building on this momentum, the conference will not only highlight fundamental advances in our understanding of disease biology but also explore their translation into the next generation of transformative therapies for cardiovascular disease.

Key Sessions

Seven sessions are planned and will highlight the following major research areas:
•    Cellular vessel wall and plaque diversity
•    Cellular metabolism, cell death and immunity
•    Transcriptional regulation in vascular cells
•    Inflammasome and other inflammatory pathways 
•    Innate immunity and macrophage biology
•    Adaptive immune mechanisms and autoimmunity
•    Immunometabolism and leukocytes
•    Lifestyle factors and vascular inflammation
•    Novel biomarkers
•    Human translational studies, drug development and clinical trials

Confirmed Invited Speakers

Vishwa Deep Dixit (Yale University)
CYSTEINE-TAURINE SHUTTLE CONTROLS INFLAMMATION
Carlos Fernández-Hernando (Yale University)
MACROPHAGE LIPID METABOLISM IN VASCULAR INFLAMMATION AND ATHEROSCLEROSIS
Ruth Frikke-Schmidt (University of Copenhagen)
INFLAMMATORY PATHWAYS – DECIPHERING GENOMICS-DRIVEN DRUG DISCOVERY OPPORTUNITIES IN ATHEROSCLEROTIC CARDIOVASCULAR DISEASE
Chiara Giannarelli (NYU Grossman School of Medicine)
SENESCENT AND CYTOTOXIC CD8+ T CELL DIFFERENTIATION IN HUMAN ATHEROSCLEROSIS
Minna Kaikkonen (University of Eastern Finland)
TRANSLATING GENETIC ASSOCIATIONS INTO FUNCTIONAL INSIGHTS IN ATHEROSCLEROSIS
Nick Leeper (Stanford University)
THE CAUSAL ROLE OF CANCER IN ATHEROSCLEROTIC PLAQUE VULNERABILITY
Peter Libby (Mass General Brigham / Harvard Medical School)
UPDATE ON CLONAL HEMATOPOIESIS AND CARDIOVASCULAR DISEASE
Esther Lutgens (Mayo Clinic)
CO-STIMULATION AND CO-INHIBITION IN ATHEROSCLEROSIS: A REBALANCING ACT
Cameron McAlpine (Icahn School of Medicine at Mount Sinai)
IMMUNOGENIC BRAIN-HEART COMMUNICATION IN ATHEROSCLEROSIS
Miriam Merad (Icahn School of Medicine at Mount Sinai)
GATEKEEPERS OF TISSUE INTEGRITY AND DRIVERS OF INFLAMMATION
Erika Pearce (Johns Hopkins University)
POLYAMINE METABOLISM IN MACROPHAGE INFLAMMATION
Fil Swirski (Icahn School of Medicine at Mount Sinai)
A CYTOKINE-DRIVEN CHOLESTEROL HANDLING MACROPHAGE CIRCUIT THAT LIMITS ATHEROSCLEROSIS
Laurent Yvan-Charvet (Côte d'Azur University)
FROM METABOLIC REWIRING TO MITOCHONDRIAL CONTROL IN ATHEROSCLEROTIC DISEASE
Ivan Zanoni (Harvard University)
MOLECULAR AND CELLULAR REGULATION OF THE FORMATION OF A PROATHEROGENIC NICHE

Target Audience

This conference will convene a select group of leading scientists from diverse disciplines, alongside participants at all career stages, to foster in-depth discussions of the latest advances in the field. By bringing together established investigators, early-career researchers, and trainees, the meeting will provide a unique platform for cross-generational exchange and cross-fertilization of ideas across scientific domains.

We particularly encourage the participation of young scientists and clinician-scientists and anticipate broad representation from multiple disciplines. The conference will be of special interest to researchers and clinician-scientists in academia, as well as colleagues from biotechnology and pharmaceutical industries, working in the areas of cardiovascular medicine and biology, immunology, metabolic diseases, immuno-metabolism, molecular and cellular biology, and epigenetics.