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We are pleased to welcome Ange Maguy from the Faculty of Medicine, University of Bern, Switzerland, and Stéphane Camus from the Paris Cardiovascular Research Center (PARCC), who have been invited by Rémi MOUNIER.
They will give a seminar on September, 23rd at 10:30 a.m. entitled: “Understanding Atrial Fibrillation: From Cellular Mechanisms to Arrhythmogenesis » and « Decoding cardiac resident macrophage dysfunction in insulin resistance and postischemic cardiac remodeling.”

The seminar will take place in Amphi 3 (3rd floor)

Ange Maguy leads the Atrial Fibrillation and Therapeutic Innovation research program at the Department of Physiology, Faculty of Medicine, University of Bern, Switzerland.

His research aims to understand how cardiac remodeling creates the substrate for arrhythmias, with a particular focus on atrial fibrillation. His work spans cellular electrophysiology, tissue remodeling and multicellular mechanisms, and combines experimental models with human cardiac samples to investigate how these processes interact during disease progression.

A major focus of his research is the development of translational models that reproduce clinically relevant forms of cardiac remodeling and allow mechanisms to be studied across scales, from individual cells to the intact heart. This approach is used to identify mechanisms linking multicellular remodeling to arrhythmogenesis and to develop therapeutic strategies that target the disease substrate rather than the arrhythmia alone.

Ange Maguy obtained his PhD in Physiology and Pharmacology from the University of Paris-Saclay and subsequently conducted postdoctoral research in cardiac electrophysiology at the Montreal Heart Institute. He received the Pfizer Research Prize in 2021 and is actively involved in European and French cardiovascular research networks.

Abstract

Atrial fibrillation is the most common sustained cardiac arrhythmia, yet the mechanisms that drive its initiation and progression remain incompletely understood. Rather than resulting from a single abnormality, atrial fibrillation emerges from the progressive interaction of electrical, structural and cellular remodeling within the atrial myocardium.

In this presentation, I will discuss experimental and translational approaches used to investigate how these changes contribute to the formation of an arrhythmogenic substrate. By combining electrophysiological studies with tissue characterization, experimental models and multi-omics approaches, we aim to connect alterations at the cellular and molecular levels with changes in atrial structure and function.

A central objective is to understand how multicellular and structural remodeling evolves into a functional arrhythmogenic substrate, and how this process can be intercepted therapeutically. Particular emphasis will be placed on how integrated studies across experimental models and human cardiac tissue can help identify mechanisms involved in disease progression and reveal new opportunities for mechanism-based therapeutic intervention.

References

Maguy A, Mahendran Y, Tardif JC, Busseuil D, Li J. Autoimmune atrial fibrillation. Circulation. 2023.

Rieger M, Dellenbach C, Vom Berg J, Beil-Wagner J, Maguy A, Rohr S. Enabling comprehensive optogenetic studies of mouse hearts by simultaneous opto-electrical panoramic mapping and stimulation. Nature Communications. 2021.

Salvarani N*, Maguy A*, De Simone SA, Miragoli M, Jousset F, Rohr S. TGF-β1 plays a pivotal role in cardiac myofibroblast arrhythmogenicity. Circulation: Arrhythmia and Electrophysiology. 2017.

Quang KL*, Maguy A*, Qi XY, Naud P, Xiong F, Tadevosyan A, Shi YF, Chartier D, Tardif JC, Dobrev D, Nattel S. Loss of cardiomyocyte integrin-linked kinase produces an arrhythmogenic cardiomyopathy in mice. Circulation: Arrhythmia and Electrophysiology. 2015.

Stéphane Camus

-PhD at Paris Centre for Cardiovascular Research (Inserm Unit 970), I showed that 1. The platelet protein thrombospondin-1 is a potent inducer of erythrocyte-derived microparticle shedding and 2. erythrocyte-derived microparticles trigger vaso-occlusive crises in sickle cell anemia by delivering heme to endothelial cells -post doc 1:Brodsky lab at the University of California, San Francisco where I was awarded a postdoctoral fellowship from the American Heart Association. In 2015, the lab was relocated to UCL (UK) where I continue investigating the function and regulation of Clathrin Heavy Chain CHC22 -maintenant : chercheur inserm laboratoire jena sébastien sylverstre et jean sébastien hulot , on Integrative physiopathology and therapy of cardiac diseases