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Cardiovascular Research 2001 49(1):11-14; doi:10.1016/S0008-6363(00)00283-2
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Dysfunctional ischemic preconditioning mechanisms in aging

Salvatore Pepe*

Cardiac Surgical Research Unit, Alfred Hospital & Baker Medical Research Institute, Monash University Faculty of Medicine, POB 6492 St. Kilda Road Central, Melbourne, Victoria 8008, Australia

* Tel.: +61-3-9522-4353; fax: +61-3-9522-4360 spepe@baker.edu.au

Received 1 November 2000; accepted 1 November 2000

The first 150 words of the full text of this article appear below.

See article by Tani et al. [7] (pages 56–68) in this issue.


   1 Introduction
 
With increased age, the adult heart undergoes numerous anatomical, ultrastructural and biochemical changes which remodel cellular structure, function and the intracellular adaptive response to pathological stress [1–6]. Compared to young adult myocardium, the senescent myocardium has a reduced capacity to tolerate post-ischemic perturbations in intracellular metabolism and ion homeostasis [1–6]. In this issue of Cardiovascular Research, Tani et al. [7] report that there is an age-linked functional decline in protein kinase C (PKC) activation, a crucial element in the cardioprotective signaling pathways triggered by ischemic preconditioning. Lethal ischemia-reperfusion injury can be attenuated by the heart's intrinsic capacity to be ‘preconditioned’ by a variety of metabolic and pharmacological stimuli, including sub-lethal episodes of ischemia itself [8]. This discovery has generated intense investigation of the preconditioning phenomena which, despite considerable variability, has been validated in a . . . [Full Text of this Article]


   2 Mediators of preconditioning
 

   3 Effect of aging on ischemic preconditioning
 

   4 Conclusion
 

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