Why the study?
Effective pharmacological treatments for cardiac valve disease are lacking, and whether the transcription factors PROX1 and FOXC2 regulate cardiac valve development and disease was unknown.
Population
Prox1 ΔVEC mice, isolated valve cells, and human MVP and aortic valve insufficiency samples
Comparison
Prox1 conditional deletion and PDGF-B pathway modulation vs controls
Design
Preclinical animal and in vitro mechanistic study with human tissue validation
Key result
Deletion of Prox1 from valvular endothelial cells in mice resulted in enlarged, myxomatous, and stenotic valves, which was partially ameliorated by pharmacological inhibition of PDGF-B signaling.
Authors
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PDGF-B inhibition merits testing in myxomatous valve disease; animal data leave human translation open.
PROX1 and FOXC2 inhibit PDGF-B expression to prevent myxomatous degeneration of heart valves, identifying PDGF-B as a potential therapeutic target for myxomatous valve disease.
Ho et al. (2023) studied Cardiac valve disease (myxomatous degeneration). Prox1 deletion (Prox1 ΔVEC) vs. Wild-type/control was evaluated on Valve structure and function (myxomatous degeneration and stenosis). Deletion of Prox1 from valvular endothelial cells in mice resulted in enlarged, myxomatous, and stenotic valves, which was partially ameliorated by pharmacological inhibition of PDGF-B signaling.
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