Publisher's Synopsis
Myocardial ischemic syndromes pose a major medical problem and a significant economic health care concern. Reperfusion, although used in the clinical arena as essential to the survival of acutely ischemic heart muscle carries with it the risk of "reperfusion injury". Therefore the salvage of additional myocardium is highly desirable. Over a decade ago, it was shown that whole body heat shock activated a powerful endogenous protective mechanism that significantly improved myocardial salvage following prolonged ischemia and reperfusion injury in the heart. A characteristic feature of this heat shock response was the expression of a family of proteins known as heat shock proteins. Many of these proteins function as molecular chaperones, helping to refold proteins denatured as a consequence of lethal injuries and facilitating the synthesis of new proteins to replace those irreparably damaged. Altered expression of these proteins has been extensively documented in association with a diverse array of diseases such as ischemia and perfusion injury, cardiac hypertrophy, fever, inflammation, metabolic diseases, infection, cell and tissue trauma, aging, and cancer. Interestingly, some studies have now shown a direct correlation of the heat shock proteins produced and the degree of myocardial protection. This book is a thorough description of the current state of knowledge of the mechanisms of heat shock proteins induced cardiac protection at the cellular and molecular level, the controversies in this growing field and the potential of treating ischemic heart disease with overexpression of heat shock proteins in patients. The book will be especially useful for investigators interested in studying tissue injury and its protection with the overexpression of heat shock proteins.
