Editorial Focus Proteasome inhibition in hypertrophied myocardium

CARDIAC REMODELING has been described as both an adaptive and a maladaptive process. The adaptive component enables the heart to maintain function in response to pressure overload and has the effect of decreasing ventricular wall stress and com-pensates for the increased workload preserving cardiac func-tion. Along with the changes in ventricular mechanics, the development of hypertrophy is accompanied by distinct qual-itative and quantitative changes in the myocardium. At the cellular level, cardiomyocyte hypertrophy is characterized by an increase in cell size, enhanced protein synthesis, multipli-cation of sarcomeres, a switch of proteins and enzymes to fetal isoforms (7), changes in intracellular Ca2 handling (2), met-abolic alterations (1), and increased rates of apoptosis (4). Left ventricular hypertrophy in response to pressure overload is primarily the result of myocyte growth, but there are als