Protective responses in the ischemic myocardium.

Acute coronary syndromes and heart failure arising as a consequence of ischemic injury to the myocardium account for a large proportion of all hospital admissions and of all causes of death in industrialized nations. Medical and surgical management of these conditions consumes enormous resources each year, but current therapeutic measures fall far short of reducing death and disability from ischemic heart disease to acceptable levels. Several recently successful advances in therapy of acute coronary syndromes are based on limiting the extent of myocardial damage that ensues following occlusion of a major coronary artery by rapid restoration of blood flow. However, many patients are not suitable candidates for thrombolytic drugs or revascularization procedures, and these approaches often are applied too late to prevent irreversible damage to the myocardium. A greater understanding of the mechanisms of ischemic injury, and of endogenous defense mechanisms, could foster additional improvements in clinical care.

[1]  G. Semenza Surviving ischemia: adaptive responses mediated by hypoxia-inducible factor 1. , 2000, The Journal of clinical investigation.

[2]  J. Woodgett,et al.  Glycogen Synthase Kinase 3β Negatively Regulates Both DNA-binding and Transcriptional Activities of Heat Shock Factor 1* , 2000, The Journal of Biological Chemistry.

[3]  Semenza Series introduction: tissue ischemia: pathophysiology and therapeutics , 2000, The Journal of clinical investigation.

[4]  S. Nigam,et al.  Genesis and reversal of the ischemic phenotype in epithelial cells. , 2000, The Journal of clinical investigation.

[5]  K. Mori Tripartite Management of Unfolded Proteins in the Endoplasmic Reticulum , 2000, Cell.

[6]  A. Dana,et al.  Adenosine A(1) receptor induced delayed preconditioning in rabbits: induction of p38 mitogen-activated protein kinase activation and Hsp27 phosphorylation via a tyrosine kinase- and protein kinase C-dependent mechanism. , 2000, Circulation research.

[7]  G Baumgarten,et al.  Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[8]  I. Benjamin,et al.  Disruption of Heat Shock Factor 1 Reveals an Essential Role in the Ubiquitin Proteolytic Pathway , 2000, Molecular and Cellular Biology.

[9]  Stuart K. Calderwood,et al.  HSP70 stimulates cytokine production through a CD14-dependant pathway, demonstrating its dual role as a chaperone and cytokine , 2000, Nature Medicine.

[10]  I. Singh,et al.  Inhibition of Tumor Necrosis Factor-α Transcription in Macrophages Exposed to Febrile Range Temperature , 2000, The Journal of Biological Chemistry.

[11]  R. Johns,et al.  Hypoxic regulation of inducible nitric oxide synthase via hypoxia inducible factor-1 in cardiac myocytes. , 2000, Circulation research.

[12]  K. Webster,et al.  Rapid activation of neutral sphingomyelinase by hypoxia-reoxygenation of cardiac myocytes. , 2000, Circulation research.

[13]  G. Semenza Cellular and molecular dissection of reperfusion injury: ROS within and without. , 2000, Circulation research.

[14]  E. Marbán,et al.  Activation of mitochondrial ATP-dependent potassium channels by nitric oxide. , 2000, Circulation.

[15]  D. Kass,et al.  Transgenic mouse model of stunned myocardium. , 2000, Science.

[16]  I. Singh,et al.  Inhibition of tumor necrosis factor-alpha transcription in macrophages exposed to febrile range temperature. A possible role for heat shock factor-1 as a negative transcriptional regulator. , 2000, The Journal of biological chemistry.

[17]  R. Hajjar,et al.  Adenoviral gene transfer of activated phosphatidylinositol 3'-kinase and Akt inhibits apoptosis of hypoxic cardiomyocytes in vitro. , 1999, Circulation.

[18]  Toshiaki Sato,et al.  Signaling in late preconditioning : involvement of mitochondrial K(ATP) channels. , 1999, Circulation research.

[19]  P. Ping,et al.  Bifunctional role of protein tyrosine kinases in late preconditioning against myocardial stunning in conscious rabbits. , 1999, Circulation research.

[20]  D. McMillan,et al.  HSF1 is required for extra‐embryonic development, postnatal growth and protection during inflammatory responses in mice , 1999, The EMBO journal.

[21]  P. Ping,et al.  The late phase of ischemic preconditioning is abrogated by targeted disruption of the inducible NO synthase gene. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[22]  R. Kitsis,et al.  The mitochondrial apoptotic pathway is activated by serum and glucose deprivation in cardiac myocytes. , 1999, Circulation research.

[23]  M. Ashraf,et al.  Role of protein kinase C in mitochondrial KATP channel-mediated protection against Ca2+ overload injury in rat myocardium. , 1999, Circulation research.

[24]  I. Benjamin,et al.  Stress-response proteins in cardiovascular disease. , 1999, American journal of human genetics.

[25]  R. Morimoto,et al.  Regulation of the Heat Shock Transcriptional Response: Cross Talk between a Family of Heat Shock Factors, Molecular Chaperones, and Negative Regulators the Heat Shock Factor Family: Redundancy and Specialization , 2022 .

[26]  Andrew D. Miller,et al.  The Expression of Constitutively Active Isotypes of Protein Kinase C to Investigate Preconditioning* , 1998, The Journal of Biological Chemistry.

[27]  R. Voellmy,et al.  Repression of Heat Shock Transcription Factor HSF1 Activation by HSP90 (HSP90 Complex) that Forms a Stress-Sensitive Complex with HSF1 , 1998, Cell.

[28]  D. McMillan,et al.  Stress (heat shock) proteins: molecular chaperones in cardiovascular biology and disease. , 1998, Circulation research.

[29]  Carl Wu,et al.  Direct sensing of heat and oxidation by Drosophila heat shock transcription factor. , 1998, Molecular cell.

[30]  P. Wong,et al.  Overexpression of human copper, zinc-superoxide dismutase (SOD1) prevents postischemic injury. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[31]  Ivor J. Benjamin,et al.  Targeted Disruption of Heat Shock Transcription Factor 1 Abolishes Thermotolerance and Protection against Heat-inducible Apoptosis* , 1998, The Journal of Biological Chemistry.

[32]  L. Brunton,et al.  Small heat shock proteins and protection against ischemic injury in cardiac myocytes. , 1997, Circulation.

[33]  I. Benjamin,et al.  Cardioprotective effects of 70-kDa heat shock protein in transgenic mice. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[34]  Carl Wu,et al.  Heat shock transcription factors: structure and regulation. , 1995, Annual review of cell and developmental biology.

[35]  S. Horie,et al.  Induction of stress proteins in cultured myogenic cells. Molecular signals for the activation of heat shock transcription factor during ischemia. , 1992, The Journal of clinical investigation.

[36]  J. Sambrook,et al.  Protein folding in the cell , 1992, Nature.

[37]  I. Benjamin,et al.  Activation of the heat shock transcription factor by hypoxia in mammalian cells. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[38]  R. Jennings,et al.  Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. , 1986, Circulation.