Cardiac hypertrophy is induced by a variety of diseases, such as
hypertension, valvular
diseases, myocardial infarction, and endocrine disorders. Although
cardiac hypertrophy may initially be a beneficial response that normalizes wall stress and maintains normal cardiac function, prolonged
hypertrophy is a leading cause of
heart failure and
sudden death. A number of studies have elucidated molecules responsible for the development of
cardiac hypertrophy, including the
mitogen-activated
protein (MAP)
kinases pathway,
Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and
calcium/
calmodulin-dependent
protein phosphatase calcineurin pathway. These molecules may be targets for
therapies designed to prevent the progression of
cardiac hypertrophy. Numerous studies have focused on characterization of the intracellular signal transduction molecules that promote
cardiac hypertrophy in order to clarify the molecular mechanisms, but there have been only a few reports on the inhibitory regulators of hypertrophic response. Recently, several molecules have attracted much attention as endogenous inhibitory regulators of
cardiac hypertrophy. Enhancement of these inhibitory regulators would also seem to be a potential approach for the pharmacological treatment of
hypertrophy. In this review, we summarize the inhibitory molecules of
cardiac hypertrophy.