he elucidation of the molecular switches which control cardiac growth and development is one of the T central problems in cardiovascular biology and medicine, with far reaching implications for the onset of cardiovascular developmental defects, the maintenance of normal cardiac structure and function, and the pathogenesis of cardiac muscle failure. Cardiogenesis can be divided arbitrarily into various stages, including cell proliferation, eel\commitment, cell differentiation, and regional specification. The final result of this complex interplay is a highly ordered structure composed of specialised tissues which form the atria, ventricles, conduction system, and valvular structures. During postnatal development the cardiac myocyte rapidly loses its ability to proliferate and subsequent growth of the heart is based on the enlargement of preexisting myocytes. When subjected to a chronic increase in haemodynamic load, the myocardium will adapt by increasing its muscle mass. For reasons incompletely understood, there appear to be limits to this compensatory response, and longstanding hypertrophy can often result in the subsequent onset of overt heart failure. A large body of work over the past two decades has shown that these distinct cardiac phenotypes can be distinguished at the physiological and biochemical level. More recently, it has also become apparent that embryonic development, postnatal growth, and adaptation of the adult heart are orchestrated by the coordinated temporal and spatial expression of cardiac muscle genes. The sequential activation of distinct subsets of muscle genes allows the myocardium to acquire its adult phenotype and specialised metabolic, contractile, and electrophysiological properties. To investigate how the myocardium acquires and maintains these distinct phenotypes, the identification of “stage-specific genetic markers” has become a prerequisite. Subsequent analysis of the regulation of the expression of these markers will allow identification of the molecular mechanisms that dictate different cardiac phenotypes. In this regard, molecular biology provides us with powerful tools that can help to unravel the molecular events that play pivotal roles in these developmental and physiological processes. During the last decade rapid advances in the application of molecular biology to cardiac research, including transient transfection, microinjection, in vivo transfection, and transgene technology (for reviews, see’’), have allowed a first glance at the regulation of molecular events and their structural implications for the fetal, adult, and hypertrophying heart.

In this review we shall discuss recent observations and current ideas concerning cardiac gene regulation and phenotype switching. Since cardiac and skeletal muscle coexpress many muscle genes and represent the major striated muscle types in mammalian systems, a brief discussion of the skeletal muscle gene programme has been included. Subsequently, we shall review molecular biological aspects that are characteristic for various stages of the cardiac muscle cell phenotype, that is, cardiogenesis, postnatal development, and hypertrophy.