Abstract

Heart failure is a worldwide health challenge representing the most common admission diagnosis in patients aged ≥65 years. It is associated with worse prognosis even compared to that of most malignancies, despite therapeutic improvements. Research efforts are underway to combat this complex disease by increasing our understanding of the underlying molecular mechanisms associated with the structural and functional abnormalities. Here we review the molecular changes associated with the fundamental derangements observed in heart failure such as the depressed myocardial contractility and relaxation, increased cardiac fibrosis, increased cardiomyocyte stiffness and profound cytoskeletal changes.