INHIBITION OF ANOXIA-INDUCED INJURY IN HEART MYOCYTES BY CYCLOSPORINE-A

被引:238
作者
NAZARETH, W [1 ]
YAFEI, N [1 ]
CROMPTON, M [1 ]
机构
[1] UNIV LONDON UNIV COLL, DEPT BIOCHEM & MOLEC BIOL, GOWER ST, LONDON WC1E 6BT, ENGLAND
关键词
HEART CELLS; ANOXIA; CYCLOSPORINE-A;
D O I
10.1016/0022-2828(91)90181-K
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cyclosporin A is a potent immunosuppressant used to prevent graft rejection. The cellular target of cyclosporin A in T lymphocytes is believed to be cyclophilin, a ubiquitous protein with peptidyl prolyl cis trans isomerase activity located in both the cytosol and mitochondria. Recently, cyclosporin A-inhibition of mitochondrial cyclophilin has been implicated in the prevention of mitochondrial dysfunction induced in vitro by Ca2+ overload and other factors potentially relevant to ischaemic cell injury. This study investigates the effect of cyclosporin A on injury to cardiomyocytes induced by substrate-free anoxia. It is shown that cyclosporin A retards progression of the injury, most probably at a late step in the injury process. © 1991.
引用
收藏
页码:1351 / 1354
页数:4
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