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(Circulation Research. 2006;99:798.)
© 2006 American Heart Association, Inc.

Editorials

Signaling Mechanisms in Ischemic Preconditioning

Interaction of PKC and MitoK_ATP in the Inner Membrane of Mitochondria

Hossein Ardehali

From the Division of Cardiology, Department of Medicine, Northwestern University Medical Center, Chicago, Ill.

Correspondence to: Hossein Ardehali, Tarry 12–725, 303 E Chicago Ave, Chicago, IL 60611. E-mail h-ardehali@northwestern.edu

See related article, pages 878–883

Key Words: mitoK_ATP • protein kinase C- • ischemic preconditioning • RACK • protein kinase G

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The cardiac "warm up" phenomenon, described more than 50 years ago in patients with coronary artery disease, refers to improvement in cardiac symptoms and physical performance following exposure to short periods of ischemia.¹ Several mechanisms, such as adaptive reduction in oxygen consumption by the ischemic myocardial region, improved oxygen supply via collateral recruitment or dilation of the stenotic vessel, and activation of an intrinsic phenomenon called ischemic preconditioning (IPC) have been proposed to account for this phenomenon. IPC refers to a process in which brief periods of ischemia improves the ability of the heart to tolerate subsequent prolonged ischemic periods.³ It was first identified in the heart in 1986 by Murry et al,² and has since been demonstrated in various experimental and animal models.³

Several triggers have been proposed for IPC, including adenosine, bradykinin, protaglandins, opiod receptors, nitric oxide, and Ca²⁺.⁴ These triggers lead to the activation of several intracellular pathways that ultimately protect myocardial cells against injury. Although the details of these pathways have not been totally characterized, mitochondria have been shown to be key mediators of IPC. Specifically, the opening of a mitochondrial channel, called the mitochondrial ATP-sensitive potassium channel or mitoK_ATP is believed to be critical for the induction of IPC; drugs that activate this channel protect against ischemia and inhibitors of mitoK_ATP reverse these protective effects.⁵

The signaling pathways that lead to the activation of mitoK_ATP are still under investigation.⁵ In a recent article, Oldenburg et al demonstrated that in isolated rabbit adult cardiomyocytes, bradykinin . . . [Full Text of this Article]

Related Article:

Mitochondrial PKC and Mitochondrial ATP-Sensitive K⁺ Channel Copurify and Coreconstitute to Form a Functioning Signaling Module in Proteoliposomes

Martin Jaburek, Alexandre D.T. Costa, Jana R. Burton, Cinthia L. Costa, and Keith D. Garlid
Circ. Res. 2006 99: 878-883. [Abstract] [Full Text] [PDF]

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