Chapter category: Heat Shock Proteins
Stress Proteins in Myocardial Protection
Heat Shock Proteins in Myocardial Protection
Edited by: Rakesh C. KukrejaISBN: 1-58706-021-3
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Chapter authors:
Richard Carroll and Derek M. Yellon
In all organisms examined heat stress results in the synthesis of a specific group of proteins known as the heat shock or stress proteins (Hsps). Cells that accumulate these proteins adapt and become resistant to further heat stress, a protection that seems directlydependent on stress protein induction. Numerous reports also suggest that stress protein accumulation is associated with protection against differing stresses in various mammalian tissues. This chapter reviews the evidence that stress proteins are directly responsible for the adaptation that increases the resistance of cells to various forms of injury. We will examine the role of stress proteins in protecting the adapted heart against both ischemic as well as non–ischemic injury. In addition we shall discuss the involvement of stress proteins in the phenomenon of ischemic preconditioning relating specifically to the delayed adaptive process that follows short coronary artery occlusions which give rise to the so called "second window of protection".
Acute myocardial infarction is the most common cause of death in the Western world. The treatment of this condition is no longer simply supportive, awaiting the complications of ischemic injury, but has entered a new era where the mortality of acute myocardial infarction can be approximately halved by thrombolytic agents and aspirin,1 with the greatest benefit seen in those treated soon after the onset of symptoms. The lack of a reduction in mortality when thrombolytic treatment is administered late is most likely due to the fact that the prolonged coronary occlusion has resulted in such severe necrosis of the myocardium that little benefit can be derived by restoring blood flow.2 Therefore any intervention that could delay the onset of tissue necrosis could buy valuable time by extending the effective temporal window for thrombolysis. Attempts to limit myocardial infarct size over the last decade with exogenous pharmacological agents have been largely unsuccessful,3 prompting us to explore the heart's endogenous protective mechanisms to ascertain if this route may provide us with the knowledge required to protect the myocardium from severe ischemic injury.
Additional chapters from this book:
Ischemia/Reperfusion Injury and Heat Shock Proteins
Junichiro Nishizawa and Kazuhiro Nagata
Ischemic heart disease or myocardial infarction remains the most prevalent cause of death in developed countries despite advances in modern medicine. Recent advances in diagnosis and treatment...
Physiological Role of Heat Shock Protein 27
Dipak K. Das and Nilanjana Maulik
Heat shock protein 27 (Hsp27) is a stress–inducible cytosolic protein that is ubiquitously present in many normal cells. The synthesis of Hsp27 is induced by heat shock and other envir...
Stress Proteins in Myocardial Protection: Culture Shock Protein, Heme Oxygenase–1 (Hsp32), Induced by Sublethal Stresses Protects the Heart Against Oxidative Stress
Shiro Hoshida
The formation of a stress protein comprises a mechanism of cell protection highly conserved in evolution. As the induction of stress proteins makes cells more tolerant towards a second, mor...
Antisense, Heat Shock Proteins and the Heart
A. A. Knowlton
Antisense technology provides a tool with which to dissect the components of the stress response. There are two known endogenous sets of protective proteins, the heat shock proteins (Hsps) and...
Preconditioning of Cardiac Myocytes: Studies Using Cultured Neonatal
Jan A. Post, Chris T.W.M. Schneijdenberg and Arie J. Verkleij
The acquisition of tolerance towards myocardial ischemia and reperfusion can be acquired by several preconditioning procedures. The original preconditioning protocol described for myocardia...
Hsp72 in the Regulation of TNF–a Production:
Xianzhong Meng
Myocardial ischemia/reperfusion induces the production of the cardiac depressant cytokine tumor necrosis factor–a (TNF–a). Macrophages (M
Hsp70 and Ischemia Tolerance in the Compromised Heart Ger J. van der Vusse
Luc H.E.H. Snoeckx, Richard N.M. Cornelussen, Robert S. Reneman and
The discovery in eukaryotic and prokaryotic organisms of a prompt and specific response to heat shock, known as the heat shock response, has stimulated the development of a complete new res...
Role of Heat Shock Proteins, Protein Kinase C and ATP-Sensitive Potassium Channel in Delayed Myocardial Protection
Rakesh C. Kukreja, Yong-Zhen Qian and Jeffery B. Hoag
Heat shock proteins (Hsp's) are one of the highly conserved proteins in existence, found in every organism.1 These proteins are synthesized quickly and intensely in response to stre...
Cardioprotection by Stress Proteins
Heat Shock Proteins in Myocardial Protection, edited by Rakesh C. Kukreja
Myocardial ischemia causes a series of changes at the intracellular level within the cardiomyocyte. These intracellular changes include changes in calcium levels, altered osmotic control, memb...
Heat Stress Proteins: A Possible Route to Myocardial Protection
Mohamed Amrani, Caroline C. Gray and Magdi H. Yacoub
Heat stress proteins (hsp) are induced by a variety of stimuli including elevated temperature,1 ischemia,2 hypoxia,3 pressure overload4 and some ...
Stress Proteins in Myocardial Protection
Richard Carroll and Derek M. Yellon
In all organisms examined heat stress results in the synthesis of a specific group of proteins known as the heat shock or stress proteins (Hsps). Cells that accumulate these proteins adapt ...
