Anna De Bartolo, Teresa Pasqua, Naomi Romeo, Vittoria Rago, Ida Perrotta, Francesca Giordano, Maria Concetta Granieri, Alessandro Marrone, Rosa Mazza, Maria Carmela Cerra, Benjamin Lefranc, Jérôme Leprince, Youssef Anouar, Tommaso Angelone, Carmine Rocca
Maladaptive cardiac hypertrophy contributes to the development of heart failure (HF). The oxidoreductase Selenoprotein T (SELENOT) emerged as a key regulator during rat cardiogenesis and acute cardiac protection. However, its action in chronic settings of cardiac dysfunction is not understood. Here, we investigated the role of SELENOT in the pathophysiology of HF: (i) by designing a small peptide (PSELT), recapitulating SELENOT activity via the redox site, and assessed its beneficial action in a preclinical model of HF [aged spontaneously hypertensive heart failure (SHHF) rats] and against isoproterenol (ISO)-induced hypertrophy in rat ventricular H9c2 and adult human AC16 cardiomyocytes; (ii) by evaluating the SELENOT intra-cardiomyocyte production and secretion under hypertrophied stimulation...
April 20, 2024: Journal of Translational Medicine