Hypertrophic growth of cardiac myocytes is a common result of different physiological and pathological stresses. It remains a subject of considerable debate whether hypertrophy is a compensatory process that becomes maladaptive in diseased hearts or a direct contributor to the pathogenesis of heart failure. Nevertheless, many types of stressors, mechanical or neural/hormonal, induce hypertrophy and this phenoytpe is an independent risk factor in heart failure. Therefore, much effort has been devoted to uncovering mechanisms of hypertrophic growth with the expectation that intercepting this process clinically may halt the disease progression of heart failure. It is firmly established that hypertrophic growth involves alterations in gene regulation, excitation-contractile coupling, extracellular matrix remodeling and energy metabolism.