Dedication: A Tribute to Dr. Jutta Schaper. Preface. Acknowledgments. I: Cardiac Adaptation and Remodelling. 1. Molecular Changes of the Myocardium After Mechanical Circulatory Support; F. Grabellus, et al. 2. Reverse Molecular Remodeling of the Failing Human Heart Following Support with a Left Ventricular Assist Device; P.M. Heerdt, D. Burkoff. 3. Stretch-Elicited Autocrine/Paracrine Mechanism in the Heart; H.E. Cingolani, et al. 4. L-Arginine at the Crossroads of Biochemical Pathways Involved in Myocardial Hypertrophy; E. Giordano, et al. 5. Signal Transduction System in Human Aortic Smooth Muscle Cell Stimulated by Pure Pressure; H. Kawaguchi, et al. 6. Role of Mitochondrial KATP Channels in Improved Ischemic Tolerance of Chronically Hypoxic Adult and Immature Hearts; F. Kolár, et al. 7. CA2+-Dependent Signaling Pathways Through Calcineurin and CA2+/Calmodlin-Dependent Protein Kinase in Development of Cardiac Hypertrophy; H. Takano, et al. 8. Calreticulin, Cardiac Development and Congenital Complete Heart Block in Children; B. Knoblach, et al. 9. Expression of Sodium-Calcium Exchanger Genes in Heart and Skeletal Muscle Development. Evidence for a Role of Adjacent Cells in Regulation of Transcription and Splicing; M. Millour, et al. 10. NA+/H+ Exchanger and Myocardial Hypertrophy; M.C. Camilión de Hurtado, et al. II: Cardiac Signal Transduction. 11. Role of the Electrogenic Na+/HVO3- Symport in the Heart; E.A. Aiello. 12. Modulation of Atrial Natriuretic Peptide (ANP)-CReceptor and Associated Signaling by Vasoactive Peptides; M.B. Anand-Srivastava, M. Boumati. 13. RAB3 Small GTP-Binding Proteins: Regulation by Calcium/Calmodulin; R.S. Sidhu, et al. 14. Novel Aspects of Mechanical Signaling in Cardiac Tissue; R. Denyer, et al. 15. Caspase Activation in a Cardiac Cell-Free Model of Apoptosis; C. Stefanelli, et al. 16. The Role of the Voltage-Sensitive Release Mechanism in Contraction of Normal and Diseased Heart; S.E. Howlett, G.R. Ferrier. 17. Role of AT1 Receptor Blockade in Reperfused Myocardial Infarction; B.I. Jugdutt. 18. Relation Between Intracellular CA2+ Concentration and Contraction in Tetanized Myocytes of Rat and Mouse; K. Hongo, et al. 19. The Role of Hydrogen Peroxide as a Signaling Molecule; M.P. Czubryt, G.N. Pierce. 20. Localized Control of Oxidative Phosphorylation within Intracellular Energetic Units in Heart Cells: A Possible Solution of Some Old Problems; V. Saks, et al. 21. Role of High Molecular Weight Calmodulin Binding Protein in Cardiac Muscle; L. Ashakumary, et al. 22. &bgr;-Adrenergic Signaling in Chronic Heart Failure &endash; Friend of Foe? C. Maack, M. Böhm. 23. Compartmentation of Lipid Rafts as a Mechanism to Regulate &bgr;-Adrenergic Receptor Signaling in Cardiomyocytes; S.F. Steinberg. 24. Role of Renin-Angiotensin System in Phospholipase C-Mediated Signaling in Congestive Heart Failure; P.S. Tappia, et al. 25. JAK/Stat Signaling in Cardiac Diseases; M.A.Q. Siddiqui, E. Mascareno. III: Genetic Approaches to Investigative Cardiac Signal Transduct
Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor mation is beginning to provide tangible targets towards manipulating cardiac func tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben eficial response under many conditions, it can be highly deleterious and inappropri ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben eficial.
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