ESC Congress 2026 - see you in Munich
The countdown to ESC Congress 2026 has begun!
From 28–31 August, we will gather in Munich for the world's largest cardiovascular congress, bringing together clinicians, scientists and healthcare professionals to share the latest advances in cardiovascular medicine and science.
This year's congress will place a special spotlight on Artificial Intelligence, highlighting how AI is rapidly becoming an increasingly powerful co-pilot in cardiovascular medicine. From accelerating scientific discovery and improving image analysis to enabling precision medicine and supporting clinical decision-making, AI is reshaping the way we investigate, diagnose and treat cardiovascular disease.
We encourage you to attend these outstanding translational and basic science sessions covering myocardial biology, metabolism, fibrosis, regenerative medicine and emerging therapeutic strategies. For more information and links to the sessions listed below, please check out our ESC Congress 2026 highlighted sessions.
- Friday, 28 August - Multicellular Crosstalk in the Heart: Relevance for Arrhythmias and Heart Failure
- Friday, 28 August - RNA and Extracellular Vesicle Therapies for Cardiovascular Disease
- Saturday, 29 August - New Tools for Discovery in Cardiology: Human Tissue Platforms Meet Artificial Intelligence
- Sunday, 30 August - Metabolism and Cardiac Dysfunction: From Mechanisms to Therapies
- Monday, 31 August - Causes and Consequences of Cardiac Fibrosis
These sessions will bring together internationally recognised experts to discuss the latest discoveries in cardiac biology, innovative technologies and novel therapeutic opportunities, providing an excellent platform for scientific exchange and networking. We look forward to seeing many of you in Munich!
Featured paper and recommended readings
In this newsletter, we highlight an editorial discussing the recent work published in Cardiovascular Research by our WG member Alice Marino together with our Chair-Elect Luc Bertrand unraveling SMIT1 as an active driver of pathological cardiac hypertrophy and fibrosis, highlighting metabolic signalling as a promising therapeutic avenue for heart failure.
- SMIT1 promotes cardiac hypertrophy and fibrosis induced by pressure overload in mice Marino A et al. Cardiovascular Research. 2026;122:578-592.
We would also like to suggest reading the following papers:
Our WG Chair Wolfgang Linke leads this brilliant study demonstrating that selective cleavage of titin profoundly disrupts cardiac mechanical homeostasis, impairing ventricular filling and triggering progressive fibrosis that ultimately culminates in heart failure. This elegant work provides new mechanistic insight into how sarcomeric integrity preserves myocardial function.
- Freundt JK et al. Selective titin cleavage disrupts cardiac mechanical homeostasis to drive heart failure and fibrosis. Nature Cardiovascular Research. 2026;5:572-587.
Recently published in the European Journal of Heart Failure, this expert consensus, authored by our Communication Coordinator Arantxa González-Miqueo, provides a comprehensive overview of the mechanisms linking hypertension and heart failure and discusses emerging strategies for prevention, diagnosis and treatment.
- Díez J et al. An expert opinion on heart failure in hypertensive heart disease. European Journal of Heart Failure. 2026;28:217–232.
Finally, this recent study in Cardiovascular Research demonstrates that endogenous YAP promotes myocardial recovery after myocarditis by suppressing IFN-γ/STAT1 signalling, thereby reducing inflammation and fibrosis while enhancing cardiac repair. These findings identify YAP as a promising therapeutic target for preventing post-myocarditis heart failure.
- Kametani Y et al. YAP plays a critical role in myocardial recovery from myocarditis by suppressing IFN-γ signaling pathway. Cardiovascular Research. 2026 [Epub ahead of print].
Stay connected
As our working group community continues to grow, we are transitioning from our LinkedIn Group to our new official LinkedIn Page, which will become our primary communication platform with improved features. The LinkedIn Group will be gradually discontinued, so we encourage all members to make the move and follow our new page to stay connected.
Please help us grow our community by inviting colleagues and collaborators with an interest in cardiovascular basic and translational science to join us.
If you would like us to highlight a recent publication, scientific initiative, funding opportunity or upcoming meetings in future newsletters, please feel free to contact Arantxa González-Miqueo.
Kind regards,
Arantxa González
News Coordinator