Key result
Activated platelets drive endothelial-to-mesenchymal transition in calcific aortic valve disease via TGF-β release.
Why the study?
Although aortic stenosis activates platelets to release mediators such as TGF-β that promote endothelial-to-mesenchymal transition, the direct contribution of platelets to the onset of aortic stenosis remains elusive.
Answers are grounded in this paper and cite their sources.
Suggests platelet targeting in CAVD; leaves open whether inhibition alters progression in patients.
Aortic stenosis (AS) is the most common valvular heart disease and results in progressive haemodynamic disturbances, readily activating platelets. Activated platelets release soluble and vesicular mediators (collectively termed platelet releasate [PR]) from their granules, including TGF-β, a prominent mediator of endothelial-to-mesenchymal transition (EndMT). Nonetheless, the direct contribution of platelets to the onset of AS remains elusive.
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Weiß et al. (2026) studied Calcific aortic valve disease / Aortic stenosis. Activated platelets / platelet releasate (including TGF-β) was evaluated on Endothelial-to-mesenchymal transition (EndMT). Activated platelets release mediators such as TGF-β that act as molecular drivers of endothelial-to-mesenchymal transition in calcific aortic valve disease.
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