Hemostasis Today

November, 2026
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Luisa Weiss: How Platelets Drive Inflammation in Aortic Valve Disease
Nov 6, 2026, 10:29

Luisa Weiss: How Platelets Drive Inflammation in Aortic Valve Disease

Luisa Weiss, Marie Skłodowska-Curie Postdoctoral Research Fellow at Brigham and Women’s Hospital, shared a post on LinkedIn:

“Two new studies exploring the role of platelets and extracellular vesicles in calcific aortic valve disease!

I am thrilled to share two recent papers from my Marie Skłodowska-Curie Actions funded project PlateCAV3D investigating how bicuspid (BAV) and tricuspid aortic valve (TAV) morphology influences platelet-mediated inflammation, extracellular vesicle biology, and endothelial dysfunction in aortic stenosis.

Paper 1 | Circulating extracellular vesicle profiles in BAV vs. TAV disease

Using an integrated approach combining flow cytometry, super-resolution microscopy, and proteomics, we provide the first comprehensive comparison of large extracellular vesicles in patients with BAV and TAV stenosis.

Our findings reveal distinct EV profiles in BAV, including increased platelet- and leukocyte-associated EV populations, altered nanoscale characteristics, and enrichment of inflammatory pathways, highlighting their potential contribution to disease pathogenesis.

Paper 2 | Platelet-endothelial crosstalk in aortic valve disease

We demonstrate that platelet-derived mediators induce valve morphology-dependent endothelial dysfunction, with BAV-derived platelet releasate triggering particularly pronounced mitochondrial dysfunction, endothelial remodeling, and inflammatory responses.

By integrating multi-omics, functional assays, and computational signaling analyses, we identify novel mechanisms linking platelet activation to valvular endothelial dysfunction and potential therapeutic targets.

Together, these studies highlight platelets and their released mediators as important contributors to aortic valve disease, providing new insights into the biological differences between BAV and TAV stenosis and opening avenues for future mechanistic and therapeutic investigations.

A huge thank you to all co-authors, collaborators, and clinical teams whose contributions made these studies possible!”

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