Induction of Heat-Shock Proteins in Ischemic Heart and Myocardial Protection

All living organisms share a common response to hyperthermia, ischemia/reperfusion, or other physiological stresses that are unfavorable to their survival through the induction df a group of protective proteins called heat-shock or stress proteins (HSPs). These proteins play essential roles as molecular chaperones under normal conditions as well as under stressed conditions. The induction of HSPs has been demonstrated to be directly involved in the acquisition of resistance to ischemia/ reperfusion injuryin the heart. Myocardial protection against ischemia/ reperfusion injuryhas been the subject of experimental and clinical research for a long time, and numerous investigators have attempted to reduce injury caused by ischemia/reperfusion. However, few pharmacological means have yet been established for effective clinical use. Therefore, it is of considerable importance to understand the mechanisms by which cells or tissues are damaged during ischemia/reperfusion, to identify compensatory responses that may augment cell survival, and to exploit methods of clinical application. In addition, there is room for improvement in strategies to protect the myocardium during high-risk cardiovascular surgery using cardiopulmonary bypass, coronary catheter intervention, or treatments for severe ischemic heart diseases, and to preserve hearts before transplantation. We summarize here the mechanisms by which the myocardium is damaged during ischemia/reperfusion, review the induction of the heat-shock response during ischemia/reperfusion in the heart, discuss the mechanisms of this induction, and present the outlook for clinical application and future perspective.