Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA.
Trends Cardiovasc Med. 1992 Nov-Dec;2(6):209-14. doi: 10.1016/1050-1738(92)90026-O.
Hokin and Hokin were the first to demonstrate that tissue inositol phospholipid (phosphoinositide, PI) turnover was increased by hormone treatment. Twenty years later, Michell published a seminal review in which he suggested a relationship between stimulated inositol phospholipid metabolism and Ca(2+) mobilization. The biochemical link between these two events was subsequently identified by Berridge and colleagues as inositol trisphosphate (InsP(3)), a Ca(2+)-mobilizing ligand that is formed by the breakdown of phosphatidylinositol bisphosphate (PIP(2)). The other product of inositol phospholipid hydrolysis, diacylglycerol, activates a Ca(2+)-sensitive phospholipid-dependent protein kinase, protein kinase C, which has been considered as a potential regulator of cardiac ion channels, inotropic state, and gene expression. This review summarizes our current state of knowledge concerning the formation of phosphoinositide-generated second messengers in cardiac cells and their potential role in mediating functional responses in the myocardium.
霍金和霍金是最早证明激素处理会增加组织肌醇磷脂（磷脂酰肌醇，PI）转化的人。20 年后，米歇尔发表了一篇重要的综述，他在综述中提出了受刺激的肌醇磷脂代谢与 Ca(2+)动员之间的关系。随后，贝里奇德和同事们确定了这两个事件之间的生化联系，即肌醇三磷酸（InsP(3)），这是一种由磷脂酰肌醇双磷酸（PIP(2)）分解形成的 Ca(2+)动员配体。肌醇磷脂水解的另一种产物，二酰基甘油，激活了一种 Ca(2+)敏感的磷脂依赖性蛋白激酶，蛋白激酶 C，它被认为是心脏离子通道、变力状态和基因表达的潜在调节剂。这篇综述总结了我们目前对心脏细胞中磷酸肌醇生成的第二信使的形成及其在介导心肌功能反应中的潜在作用的了解。
