Abstract
Left ventricular assist devices remain a major step forward for end-stage heart failure patients awaiting transplantation. We investigated the molecular basis of the longitudinal effect of left ventricular assist device implantation in both ischemic and nonischemic cardiomyopathy patients. The results revealed a common signature of 13 genes associated with glucocorticoid receptor overexpression pretransplantation, independent of the etiology. Four key molecular hub genes from this signature were highlighted, involved respectively in metabolic plasticity (PDK4), limited inflammation (FKBP5 and ZBTB16), and repair (FOXO3). It shows, however, that these pathways contribute to cardiac homeostasis.