title: Inhibition of anoxia-induced injury in heart myocytes by cyclosporin A.
abstract: 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.
authors.affiliation: Department of Biochemistry and Molecular Biology, University College London, UK.
authors.forename: W
authors.initials: W
authors.lastname: Nazareth
authors.forename: N
authors.initials: N
authors.lastname: Yafei
authors.forename: M
authors.initials: M
authors.lastname: Crompton
mesh_terms: D000818:Animals; D016572:Cyclosporine / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000187:drug effects*; D009206:Myocardium / Q000473:pathology*; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D016572:Cyclosporine; D010100:Oxygen