Molecular Mechanisms of Cardiac Hypertrophy and FailureCRC Press, 29 nov 2005 - 812 páginas This title reviews current knowledge of the mechanisms contributing to heart failure. Editor Richard Walsh and an internationally renowned team of contributors discuss key advances in molecular and cell biology, biochemistry, and pharmacology, focusing on advances that have a direct bearing on current clinical studies. It highlights developments across a broad range of disciplines, with in-depth coverage of each topic providing background and perspective on current literature. By setting new advances in a broader context, this text allows readers to compare different ideas and evaluate their importance in their own areas of research or clinical practice. |
Índice
Section I Mechanisms for Cardiac Hypertrophy | 1 |
Section II Mechanisms for Contractile Depression | 225 |
Section III Arrhythmogenesis | 467 |
Section IV Genetic Basis for Cardiomyopathy | 610 |
897 | |
Otras ediciones - Ver todo
Molecular Mechanisms of Cardiac Hypertrophy and Failure Richard A. Walsh No hay ninguna vista previa disponible - 2019 |
Molecular Mechanisms of Cardiac Hypertrophy and Failure Richard A. Walsh No hay ninguna vista previa disponible - 2005 |
Términos y frases comunes
abnormalities acid actin activation addition adult altered apoptosis arrhythmia associated atrial binding Biol Chem Ca2+ calcium cardiac hypertrophy cardiac myocytes Cardiol cardiomyocytes cardiovascular cause cell cellular changes channel Circ Res Circulation clinical common complex conduction contractile coronary coupling cytoplasmic death decreased defects dilated cardiomyopathy disease disorders domain dysfunction effects et al evidence expression factor failing Figure function gene genetic growth heart failure human hypertrophic cardiomyopathy identified important increased induced infarction inhibition interactions intracellular involved lead left ventricular levels mechanisms mediated membrane mice mitochondrial molecular mouse muscle muscular dystrophy mutations myocardial myocardial infarction myocardium myosin normal observed occurs pathways patients phenotype phosphorylation Physiol potential present protein recent receptor reduced region regulation release remodeling reported response risk role sarcomere showed shown signaling skeletal specific stimulation structure studies suggest syndrome tissue transcription