University of Rochester has received a USD 2.38 million NIH R01 grant from the National Heart, Lung, and Blood Institute (NHLBI) to investigate how protein kinase D3 (PKD3) regulates endothelial-to-mesenchymal transition (EndMT) in mitral valve prolapse (MVP), a valvular heart condition.
The award, running from August 2026 through May 2030, responds directly to NHLBI's Notice of Special Interest NOT-HL-23-079, which sought applications focused on heart valve disease mechanisms. Principal investigator Zheng-Gen Jin and colleagues will use global and endocardial-specific PKD3 knockout mouse models to map how PKD3 loss drives pathological EndMT, the process by which endothelial cells acquire mesenchymal characteristics, secreting proinflammatory mediators and extracellular matrix proteins that disrupt valve architecture. The research will incorporate single-cell RNA sequencing and transcriptomics to resolve cell-state changes at high resolution, alongside in vitro, ex vivo, and in vivo functional assays. The team's prior work linked PKD3 to vascular endothelial growth factor (VEGF) signaling in endothelial cells.
MVP currently lacks approved pharmacological therapies; surgical repair or replacement remains the standard intervention for severe cases. The NHLBI's targeted funding notice reflects institutional interest in expanding the molecular understanding of valve disease to identify druggable pathways upstream of structural deterioration.
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