Mechanotransduction in cardiomyocyte hypertrophy.

The study of ventricular hypertrophy has recently been a fruitful research area. From studies principally in neonatal rat ventricular myocytes in primary culture but now increasingly in transgenic mice, the molecular mechanisms involved in this important pathophysiological adaptation are becoming clearer.1 In culture, cardiomyocyte hypertrophy is characterized by numerous transcriptional and morphological changes, including increased expression of atrial and B-type natriuretic peptides (ANP and BNP, respectively), increased b-myosin heavy chain (b-MHC) expression, and increased sarcomere deposition.1 Similar changes are evident in hypertrophied hearts in vivo, where increased sarcomere deposition in particular allows cardiomyocytes to accommodate demands for elevated contractile power.