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Cardiovascular Research 2007 73(4):623-625; doi:10.1016/j.cardiores.2007.01.004
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Copyright © 2007, European Society of Cardiology

The myocardial no-reflow phenomenon: Role of {delta}PKC

Gregory J. Wilsona,b,c,* and Roberto J. Diaza,b

aDivision of Cell Biology, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8
bDepartment of Laboratory Medicine, Division of Pathology, Hospital for Sick Children, Toronto, ON, Canada
cDepartments of Laboratory Medicine and Pathobiology, Physiology and Surgery, University of Toronto, ON, Canada

* Corresponding author. Division of Cell Biology, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8. Tel.: +1 416 813 2095; fax: +1 416 813 5965. Email address: gregory.wilson@sickkids.ca

Received 4 January 2007; accepted 8 January 2007

The first 10% of the full text of this article appears below.

See article by Ikeno et al. [1] (pages 699–709) in this issue.

In the paper "Impaired perfusion after myocardial infarction is due to reperfusion-induced {delta}PKC-mediated myocardial damage" by Ikeno et al. [1], Dr. Daria Mochly-Rosen's group at Stanford University have demonstrated a novel molecular interventional strategy, targeted inhibition of the {delta} isoform of protein kinase C ({delta}PKC), to treat the post-ischemic no-reflow phenomenon in the myocardium using both mouse and pig models. This they achieved by either expressing a {delta}PKC-specific translocation inhibitor protein fragment, {delta}V1-1, only in cardiomyocytes in a transgenic crystalloid perfused mouse ex-vivo acute global myocardial ischemia (30 min)/reperfusion (120 min) model or through intra-coronary delivery of the TAT-conjugated synthetic peptide {delta}V1-1 during the last minute of ischemia in a porcine in-vivo regional (LAD) myocardial ischemia . . . [Full Text of this Article]


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