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Delineating PLATElet-induced sex-specific responses in Calcific Aortic Valve disease using 3D-bioprinting and proteomics.

Project description

Platelet-mediated mechanisms in aortic valve disease

Calcific aortic valve disease (CAVD) is characterised by pathological thickening and calcification of the aortic valve. Accumulating evidence indicates that CAVD progression exhibits a sex bias and morphology variations, but the underlying aetiology remains poorly understood. With the support of the Marie Skłodowska-Curie Actions programme, the PlateCAV-3D project aims to investigate the role of activated platelets in early CAVD. The hypothesis is that platelet mediators like TGF-β induce endothelial-to-mesenchymal transition and contribute to CAVD. Researchers will follow an interdisciplinary approach to identify and validate platelet-derived factors of CAVD. The study is expected to lead to new therapeutic targets and alternative interventions to valve replacement surgery.

Objective

Calcific aortic valve disease (CAVD) is an increasing global health burden. Once symptomatic and untreated, CAVD confers a 2-year mortality rate of ~50%. Crucially, costly and highly specialised valve replacement surgery remains the only treatment. Additionally, while male and female patients present with calcific or fibrotic tissue degeneration, respectively, experimental studies mostly use male models. The rising disease burden, lack of understanding of differential pathophysiological mechanisms underlying CAVD onset and progression, and inequality in accessing surgical intervention impose the need to uncover novel therapeutic targets to delay disease development. Haemostatic alterations, including platelet activation, are implicated in CAVD, and may particularly compromise patients with bicuspid vs. tricuspid valves. Endothelial-to-mesenchymal transition of valvular endothelial cells is a hallmark of CAVD onset and potently induced by platelet-derived mediators such as TGF-β, suggesting the direct involvement of activated platelets. The differential platelet-mediated mechanisms underlying both the valve morphology- and sex-specific disease
pathophysiology remain elusive. We will perform unbiased global proteomics to identify novel platelet-derived mediators in the onset of CAVD. These mediators will be used to induce CAVD in a biologically relevant, sex-specific 3D bioprinted in vitro model. By combining histopathology, imaging, proteomics, and bioinformatics, PlateCAV-3D will characterise the contribution of platelets to the onset of CAVD and infer valve morphology- and sex-specific disease trajectories to uncover novel therapeutic targets. Identification of patient-specific therapeutic target candidates provides the opportunity to design clinical trials to decelerate disease onset/progression and ultimately diminish the need for surgical intervention, globally decreasing health care costs, and eradicating the inequality in access to interventional therapies.

Fields of science (EuroSciVoc)

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Keywords

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Programme(s)

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Topic(s)

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Funding Scheme

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HORIZON-TMA-MSCA-PF-GF - HORIZON TMA MSCA Postdoctoral Fellowships - Global Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2024-PF-01

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Coordinator

UNIVERSITY COLLEGE DUBLIN, NATIONAL UNIVERSITY OF IRELAND, DUBLIN
Net EU contribution

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€ 426 533,76
Total cost

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No data

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