Key result
Calcific aortic valve disease is an active pathogenic process driven by the re-activation of developmental signaling pathways such as TGF-beta, BMP, Wnt, Notch, and Sox9.
This review emphasizes the reactivation of embryonic valvulogenesis and bone development signaling pathways in the pathogenesis of calcific aortic valve disease, providing a framework for developing non-surgical therapies.
Suggests developmental pathways as therapeutic targets in calcific aortic valve disease; leaves open clinical translation pending targeted trials.
PURPOSE OF REVIEW: This review aims to highlight the past and more current literature related to the multifaceted pathogenic programs that contribute to calcific aortic valve disease (CAVD) with a focus on the contribution of developmental programs. RECENT FINDINGS: Calcification of the aortic valve is an active process characterized by calcific nodule formation on the aortic surface leading to a less supple and more stiffened cusp, thereby limiting movement and causing clinical stenosis. The mechanisms underlying these pathogenic changes are largely unknown, but emerging studies have suggested that signaling pathways common to valvulogenesis and bone development play significant roles and include Transforming Growth Factor-β (TGF-β), bone morphogenetic protein (BMP), Wnt, Notch, and Sox9. This comprehensive review of the literature highlights the complex nature of CAVD but concurrently identifies key regulators that can be targeted in the development of mechanistic-based therapies beyond surgical intervention to improve patient outcome.
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Dutta et al. (2018) conducted a review in Calcific Aortic Valve Disease. Calcific aortic valve disease is an active pathogenic process driven by the re-activation of developmental signaling pathways such as TGF-beta, BMP, Wnt, Notch, and Sox9.
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