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Protein Kinase C - the Key-Enzyme in Ischemic Preconditioning?

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Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 194))

Abstract

Ischemic preconditioning of the heart is a phenomenon whereby one or more brief episodes of ischemia render the heart more resistant to injury from a subsequent longer ischemic insult. Preconditioning was originally described a decade ago as a protective intervention that reduced the area of necrosis from a standardized ischemic insult.1 Subsequently numerous studies have shown that preconditioning can also provide protection against other detrimental effects of ischemia, such as arrhythmia and possibly even postischemic contractile dysfunction as occurs in the stunned myocardium.2,3 There is of course no proof that the mechanisms responsible for the protective effects against necrosis, recovery of function and arrhythmias are all the same. In fact current evidence would suggest that the anti-arrhythmic and the anti-infarct effects are accomplished by quite different pathways. Ischemic preconditioning against infarction has been confirmed in every animal model that has been studied and there is considerable evidence, albeit indirect, that ischemic preconditioning also occurs in man.4 The actual mechanism of ischemic preconditioning has not yet been determined although considerable light has been shed on the signal transduction systems that are involved. Investigations in ischemic preconditioning have revealed that protection against infarction, at least in some species, is mediated through activation of protein kinase C (PKC), but it is not yet known how PKC is being activated nor what the final effector might be.5,6

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Downey, J.M., Weinbrenner, C. (1997). Protein Kinase C - the Key-Enzyme in Ischemic Preconditioning?. In: Mentzer, R.M., Kitakaze, M., Downey, J.M., Hori, M. (eds) Adenosine, Cardioprotection and Its Clinical Application. Developments in Cardiovascular Medicine, vol 194. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-8736-5_6

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