UC Louvain

Study by A. Marino: Growing body of evidence associate changes in cardiac metabolism to the pathogenesis and progression of heart failure. Plasmatic myo-inositol is high in patients with failing hearts, suggesting that it may participate in heart failure development. Myo-inositol transporter SMIT1 is expressed in cardiac fibroblasts and cardiomyocytes. Our hypothesis is that myo-inositol/SMIT1 axis favor hypertrophy and fibrosis, thus we aim to establish its impact on left ventricular remodeling and heart failure.