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BL
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| Record Number
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725726
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| Doc. No
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b545447
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| Main Entry
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Richard A Walsh
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| Title & Author
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Molecular Mechanisms of Cardiac Hypertrophy and Failure.\ Richard A Walsh
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| Publication Statement
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London: Informa Healthcare, 2005
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| Page. NO
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(1038 pages)
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| ISBN
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0203503244
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: 9780203503249
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| Contents
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Book Cover; Half-Title; Title; Copyright; Dedication; Contents; Contributors; Preface; Acknowledgements; Abbreviations; Color Plate Section; Section I Mechanisms for Cardiac Hypertrophy; 1. Mechanisms of Normal Cardiovascular Growth and Development; 2. Cardiomyocyte Cell Cycle Control; 3. Molecular Mechanisms of Cardiac Myocyte Death; 4. Transcription Factors and Hypertrophy; 5. G Protein-coupled Receptor Activation; 6. Mechanotransduction in Cardiomyocyte Hypertrophy; 7. Extracellular Matrix; 8. Physiological Versus Pathological Cardiac Hypertrophy; 9. Alterations in Signal Transduction. 10. Cell-based Therapies for Cardiac Regeneration and Repair11. Oxidative Stress in the Regulation of Myocardial Hypertrophy and Failure; Section II Mechanisms for Contractile Depression; 12. Normal and Abnormal Excitation-contraction Coupling; 13. Normal and Abnormal Calcium Homeostasis; 14. Mechanisms of Reversible Ischemic Dysfunction; 15. Cardiac Remodeling; 16. The Role of Inflammatory Mediators in Cardiac Hypertrophy, C.
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| Abstract
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The major impetus for the design and execution of Molecular Mechanisms for CardiacHypertrophy and Failure has been the remarkable insights into the pathogenesis ofabnormal cardiac growth and function that have been derived from the application ofmolecular and cellular approaches to this problem over the past decade. The syndrome ofcongestive heart failure is a major and growing public health problem in both developedand developing countries. In developed countries, the aging of our populations hasallowed more protracted impacts of genetic and environmental factors that have resultedin the cont.
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| Subject
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Heart -- Hypertrophy -- Molecular aspects.
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| LC Classification
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RC682.9R534 2005
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| Added Entry
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Richard A Walsh
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