Abstract
Oxygen free radicals have been demonstrated to have the capacity to cause cardiac contractile dysfunction [1–4]. It is well known that cardiac contraction is produced by the interaction between actin and myosin and that the energy for the contraction is supplied through the myosin ATPase reaction [5]. Myofibrillar creatine kinase has been demonstrated to be functionally coupled to myosin ATPase [6–8] and serves as an important intramyofibrillar ATP-regenerating system (phosphocreatine energy shuttle) [5]. Therefore, alterations in myofibrillar creatine kinase activity may disturb energy utilization by the myocardium and may result in contractile dysfunction. In fact, it has been reported that inhibition of creatine kinase activity can result in dysfunction of the heart, especially at increased work loads [9].
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Kaneko, M., Matsumoto, Y. (1996). Changes in Contractile Proteins under Oxidative Stress. In: Dhalla, N.S., Singal, P.K., Takeda, N., Beamish, R.E. (eds) Pathophysiology of Heart Failure. Developments in Cardiovascular Medicine, vol 168. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1235-2_10
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DOI: https://doi.org/10.1007/978-1-4613-1235-2_10
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