Intracellular signaling pathways in cardiac myocytes induced by mechanical stress

Abstract

Mechanical stress is a major cause for cardiac hypertrophy. Although the mechanisms by which mechanical load induces cardiomyocyte hypertrophy have long been a subject of great interest for cardiologists, the lack of a good in vitro system has hampered the understanding of the biochemical mechanisms. For these past several years, however, an in vitro neonatal cardiocyte culture system has made it possible to examine the biochemical basis for the signal transduction of mechanical stress. Passive stretch of cardiac myocytes cultured on silicone membranes activates phosphorylation cascades and induces the expression of specific genes as well as the increase in protein synthesis. Although an important question regarding how mechanical stimulus is converted into biochemical signals remains unanswered, cultured cardiac myocytes may be a good model to examine the signal transduction pathways of mechanical stress.