Exercise, heat shock proteins, and myocardial protection from I-R injury

Powers S., Locke M., Demirel H.

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE, vol.33, no.3, pp.386-392, 2001 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Review
  • Volume: 33 Issue: 3
  • Publication Date: 2001
  • Doi Number: 10.1097/00005768-200103000-00009
  • Journal Name: MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.386-392
  • Keywords: stress proteins, heart, skeletal muscle, gene expression, DNA-BINDING ACTIVITY, HEME OXYGENASE GENE, TRANSCRIPTION FACTOR, STRESS-PROTEINS, DIFFERENTIAL EXPRESSION, SKELETAL-MUSCLE, CHAPERONE YDJ1, RNA-POLYMERASE, MESSENGER-RNA, HSP70
  • Hacettepe University Affiliated: Yes

Abstract

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.