Platelet-endothelial crosstalk drives distinct endothelial dysfunction in bicuspid aortic valve disease

Platelet releasate from bicuspid aortic valve (BAV) patients induces a substantially more pronounced endothelial dysfunction than tricuspid aortic valve (TAV) releasate, with mitochondrial dysfunction as a central feature.

• Why it matters: BAV hemodynamics likely alters platelet and valvular endothelial cell signaling, but whether platelet-derived signals shape morphology-specific endothelial dysfunction in aortic stenosis was unknown.
• What they did: Platelets and valvular endothelial cells were collected from BAV or TAV patients undergoing valve replacement for aortic stenosis; platelet releasate was profiled and tested on VECs using molecular, multi-omic, functional, and computational ligand-receptor analyses.
• The result: BAV-derived releasate triggered widespread molecular reprogramming, mitochondrial depolarization, altered mitochondrial dynamics, enhanced VEC migration, and increased neutrophil adhesion and chemotaxis, identifying candidate platelet-to-endothelial signaling axes for therapeutic targeting.

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