Ins(1,4,5)P3 and cardiac dysfunction

被引：29

作者：

Woodcock, EA

Matkovich, SJ

Binah, O

机构：

[1] Baker Med Res Inst, Cellular Biochem Lab, Prahran, Vic, Australia

[2] Technion Israel Inst Technol, Bernard katz Ctr Cell Biophys, Rappaport Family Inst Res Med Sci, Haifa, Israel

来源：

CARDIOVASCULAR RESEARCH | 1998年 / 40卷 / 02期

关键词：

arrhythmia (mechanisms); calcium (cellular); signal transduction; reperfusion; immunology;

D O I：

10.1016/S0008-6363(98)00187-4

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

There is now substantial evidence that Ins(1,4,5)P3, by virtue of its role in Ca2+ release, can initiate electro-physiological disturbances which develop into cardiac arryhtmias, and in addition appears to be involved in the progression of the cardiomyocytes to apoptosis. Therapeutic regimens targeting the generation or the actions of Ins(1,4,5)P3 may thus prove beneficial in treating or preventing a number of different cardiac pathologies.

引用

页码：251 / 256

页数：6

共 68 条

[1] INOSITOL PHOSPHATE RELEASE AND METABOLISM DURING MYOCARDIAL-ISCHEMIA AND REPERFUSION IN RAT-HEART [J].