20 Expression and Function of Stress Proteins in the Ischemic Heart

Abstract

I. INTRODUCTION
The goal of this chapter is to summarize current understanding of the regulation and function of heat shock proteins in the ischemic heart. The clinical context in which this subject is discussed is an important one. Despite recent therapeutic advances, ischemic heart disease remains the leading cause of death and disability in industrialized nations. Coronary thrombosis, occurring against a backdrop of chronic atherosclerosis, leads rapidly to cell death within the heart (Reimer and Jennings 1988). If a sufficient mass of myocardium is injured, the patient will succumb either to inadequate pump function of the heart or to lethal dysrhythmias that accompany this condition. The progression to cellular necrosis is not, however, instantaneous, as shown by the beneficial effects of thrombolytic therapy delivered within the first few hours (Braunwald and Sobel 1988). Therefore, efforts to understand the mechanisms by which cells are damaged during ischemia and to identify compensatory or adaptive responses that may augment cell survival are of paramount importance (Williams and Benjamin 1991).

General and specific features of the molecular biology, genetics, and biochemistry of heat shock proteins are discussed in detail in other chapters in this volume and will not be reiterated here. Rather, our discussion focuses explicitly on the heart and on efforts to understand the role of heat shock proteins in the complex series of events triggered by ischemia within the myocardium. Since terms used by cardiovascular investigators may be unfamiliar to molecular biologists and other scientists interested in heat shock proteins, some definitions...