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Signaling pathways in ischemic preconditioning.

James M Downey1, Amanda M Davis, Michael V Cohen

  • 1Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA.

Heart Failure Reviews
|May 23, 2007
PubMed
Summary
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Ischemic preconditioning protects the heart from damage by activating protein kinase C (PKC). This protective state is triggered by adenosine, bradykinin, and opioids, ultimately inhibiting harmful mitochondrial pores.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Signaling

Background:

  • Ischemic preconditioning confers resistance to heart infarction caused by ischemia/reperfusion injury.
  • Significant progress has been made in understanding the molecular mechanisms underlying preconditioning over the past two decades.

Purpose of the Study:

  • To elucidate the parallel signaling pathways triggered by adenosine, bradykinin, and opioids in activating protein kinase C (PKC).
  • To identify the key survival kinases and their role in inhibiting mitochondrial permeability transition pore formation during reperfusion.

Main Methods:

  • Investigated the signaling cascades involving phosphatidylinositol 3-kinase (PI3-kinase), Akt, nitric oxide synthase, guanylyl cyclase, and protein kinase G (PKG).
  • Examined the role of epidermal growth factor receptor transactivation in opioid-mediated PI3-kinase activation.

Related Experiment Videos

  • Assessed the activation of survival kinases Akt and ERK and their downstream targets like GSK-3beta.

    • Main Results:

    • Adenosine, bradykinin, and opioids activate PKC through distinct pathways.
    • Bradykinin and opioid pathways involve PI3-kinase, Akt, and downstream signaling molecules.
    • Protection against ischemia/reperfusion injury is mediated by Akt and ERK-dependent inhibition of mitochondrial permeability transition pore formation.
    • Protective signals are required for approximately one hour post-reperfusion.

    Conclusions:

    • Ischemic preconditioning involves complex, parallel signaling pathways converging on PKC activation.
    • Survival kinases Akt and ERK play a crucial role in preventing mitochondrial damage during reperfusion.
    • The protective effects of preconditioning are transient, lasting only about an hour.