Molecular Cardiology Division, Third Department of Medicine, University of Tokyo School of Medicine, Tokyo 113, Japan.
Trends Cardiovasc Med. 1994 May-Jun;4(3):117-21. doi: 10.1016/1050-1738(94)90063-9.
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.
机械应力是引起心肌肥厚的主要原因。尽管机械负荷引起心肌细胞肥厚的机制一直是心脏病学家非常感兴趣的课题，但缺乏良好的体外系统阻碍了对生化机制的理解。然而，在过去的几年中，一种体外新生大鼠心肌细胞培养系统使得研究机械应激信号转导的生化基础成为可能。在硅酮膜上培养的心肌细胞的被动拉伸激活磷酸化级联反应，并诱导特定基因的表达以及蛋白质合成的增加。尽管关于机械刺激如何转化为生化信号的一个重要问题仍未得到解答，但培养的心肌细胞可能是研究机械应激信号转导途径的良好模型。
