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Cardiovascular Research 2003 59(1):1-6; doi:10.1016/S0008-6363(03)00337-7
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Mitochondrial plasticity in classical ischemic preconditioning—moving beyond the mitochondrial KATP channel

Jan Minners, Christopher J. McLeod and Michael N. Sack*

Hatter Institute for Cardiology Research and MRC Inter-University Cape Heart Group, University of Cape Town Medical School, Cape Town, South Africa

sackm{at}nhlbi.nih.gov

* Corresponding author. Cardiovascular Branch, 10/7B15 National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1650 USA. Tel.: +1-301-451-9741; fax: +1-301-402-0888.

Ischemic preconditioning is a powerful biologic phenomenon that activates innate cell survival programs to protect the heart from ischemic injury. The preponderance of research into classical ischemic preconditioning has focused on signaling pathways orchestrating cardioprotection. Conceptually classified into triggers, mediators and end effectors of preconditioning multiple distinct signaling pathways appear to ‘converge’ on the mitochondria possibly via activation of the mitochondrial ATP-sensitive potassium (mKATP) channel. The mechanisms by which mKATP channel activation induces preconditioning are incompletely elucidated but include perturbations of mitochondrial architecture and function. Since evidence invoking the mKATP channel has almost exclusively been based on studies using diazoxide and 5-hydroxydecanote the finding that these two compounds have mitochondrial effects independent of the mKATP channel has initiated a controversy regarding the exclusivity of this particular channel in preconditioning. A concerted effort to characterize the mitochondrial phenotype is important to advance our understanding of the mechanistic events that underlie the robust cardioprotective phenotype unmasked by preconditioning. The purpose of this review is to collate the information available on mitochondrial biology associated with classical preconditioning, to delineate the distinct temporal presentation of these mitochondrial perturbations, to reassess the role of the mitochondrial KATP channel and to propose a working model integrating the mitochondrial adaptations into the biology driving this cyto-protective phenotype.

KEYWORDS Preconditioning; Mitochondria; K-ATP channel; Energy metabolism; Infarction


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