Key result
Inhibiting glucose metabolism and hexosamine biosynthesis disrupts inflammatory protein maturation and monocyte adhesion in valve cells.
Why the study?
Valve endothelial cell metabolism has received less attention than valve interstitial cell metabolism, despite both resident valve cell types encountering inflammatory cues in early calcific aortic valve disease.
Does inhibiting glycolysis and hexosamine biosynthesis reduce inflammatory protein expression and monocyte recruitment in human aortic valve cells?
Does inhibiting glycolysis and hexosamine biosynthesis reduce inflammatory protein expression and monocyte recruitment in human aortic valve cells?
Glycolysis and hexosamine biosynthesis are crucial for inflammatory protein maturation and monocyte recruitment in human aortic valve cells, highlighting potential metabolic targets for early-stage calcific aortic valve disease.
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Should not change valve disease care; leaves open whether glycolytic inhibition will prove therapeutic in patients.
Sánchez‐Bayuela et al. (2026) studied Calcific aortic valve disease. Inhibition of glucose metabolism and hexosamine biosynthesis vs. Uninhibited state was evaluated on Inflammatory protein expression, glycoprotein maturation, and monocyte adhesion. Inhibiting glucose metabolism and hexosamine biosynthesis in human aortic valve cells disrupted inflammatory protein maturation and impaired monocyte rolling and adhesion.
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