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ACKR1-high endothelial cells enhance CXCL8 responsiveness and reveal a therapeutic entry point in calcific aortic valve disease

29 August 2026 (14:40 - 14:50)
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Congress Presentation Part of: Molecular and genetic basis for aortic valve disease Pathophysiology and Mechanisms ESC2026 Premium Access ESC Congress 2026 European Society of Cardiology

About the speaker

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Doctor Xu Nan Guo

Beijing AnZhen Hospital affiliated to Capital Medical University, Beijing (China)

5 More presentations in this session

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One locus, three phenotypes: LPA as the common genetic driver of early aortic valve calcification, coronary artery calcification and carotid plaque
Doctor A. Wang Gottlieb (Stockholm, SE)
Abstract Slides
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CD44---targeted rosuvastatin delivery attenuates valvular fibrotic remodelling in calcific aortic valve disease
Doctor X. Yuan (Beijing, CN)
Abstract Slides Video
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Disruption of the basement membrane underlies common pathogenesis of valvular heart diseases revealed by a pan-valvular single-cell atlas
Doctor H. Shi (Wuhan, CN)
Abstract Slides
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Hsp90α attenuates calcific aortic valve disease by upregulation HIF-1α and suppressing VIC osteogenesis
Professor Y. Chen (Beijing, CN)
Abstract Slides Video
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Spatiotemporal dynamics of interleukin 6 in calcific aortic valve disease: a multi-omics and translational study
Doctor S. Shu (Beijing, CN)
Abstract Slides

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Molecular and genetic basis for aortic valve disease
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The Event

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ESC Congress 2026

29 August 2026 14:40 CET
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