Exercise, heat shock proteins, and myocardial protection from I-R injury.
Heat shock proteins (HSPs) play a critical role in maintaining cellular homeostasis and protecting cells during episodes of acute stress. Specifically, HSPs of the 70 kDa family (i.e., HSP72) are important in preventing ischemia-reperfusion induced apoptosis, necrosis, and oxidative injury in a variety of cell types including the cardiac myocyte. Evidence indicates that HSP72 may contribute to cellular protection against a variety of stresses by preventing protein aggregation, assisting in the refolding of damaged proteins, and chaperoning nascent polypeptides along ribosomes. Endurance exercise is a physiological stress that can be used to elevate myocardial levels of HSP72. It is now clear that endurance exercise training can elevate myocardial HSP72 by 400-500% in young adult animals. Importantly, an exercise-induced elevation in myocardial HSPs is associated with a reduction in ischemia-reperfusion (I-R) injury in the heart. Although it seems likely that exercise-induced elevations in myocardial levels of HSPs play an important role in this protection against an I-R insult, new evidence suggests that other factors may also be involved. This is an important area for future research.
Powers
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Department of Exercise and Sport Sciences and Physiology, Center for Exercise Science, University of Florida, Gainesville, FL 32611, USA. spowers@hhp.ufl.edu
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D017209:Apoptosis; D015444:Exercise / Q000502:physiology*; D005786:Gene Expression Regulation; D018882:Heat Stress Disorders; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000494:pharmacology; D006801:Humans; D018482:Muscle, Skeletal / Q000502:physiology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D018384:Oxidative Stress; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*
D006360:Heat-Shock Proteins