Cardiac Remodeling Molecular Mechanisms /

• Συγγραφή απο Οργανισμό/Αρχή: SpringerLink (Online service)
• Άλλοι συγγραφείς: Jugdutt, Bodh I. (Επιμελητής έκδοσης), Dhalla, Naranjan S. (Επιμελητής έκδοσης)
• Μορφή: Ηλεκτρονική πηγή Ηλ. βιβλίο
• Γλώσσα: English
• Έκδοση: New York, NY : Springer New York : Imprint: Springer, 2013.
• Σειρά: Advances in Biochemistry in Health and Disease ; 5
• Θέματα: Medicine.; Human physiology.; Molecular biology.; Cardiology.; Medical biochemistry.; Biochemistry.; Medicine & Public Health.; Medical Biochemistry.; Human Physiology.; Molecular Medicine.; Biochemistry, general.

 The main objective of Cardiac Remodeling: Molecular Mechanisms is to summarize the major research advances in molecular, biochemical and translational aspects of cardiac remodeling over the last 2 to 3 decades under one cover and touch on future directions. It provides a high profile and valuable publication resource on molecular mechanisms of cardiac remodeling for both the present and future generations of researchers, teachers, students and trainees. This book should stimulate future translational research targeted towards discovery and development for preventing, limiting and reversing bad remodeling over the next few decades, with the ultimate goal of preventing progression to systolic and/or diastolic heart failure. The chapters suggest potential novel strategies that should receive attention for translating basic research knowledge to application in patients at the bedside. 

 Part I: Molecular mechanisms of remodeling in pressure and volume overload hypertrophy and ehart failure -- β-adrenergic receptor signaling pathway in heart failure -- Remodeling of potassium channels in cardiac hypertrophy -- Role of gender in Ca2+ cycling and cardiac remodeling due to heart failure -- The failing heart: is it an inefficient engine or an engine out of fuel? -- Regulation of cardiac hypertrophic remodeling by the USP15/SLIM1 pathway -- Role of galectin-3 pathways in the pathogenesis of cardiac remodeling and heart failure -- A mitochondriocentric pathway to cardiomyocyte necrosis:  an upstream molecular mechanism in myocardial fibrosis -- The ACE2/Ang (1-7) pathway in cardiac remodeling due to pressure-overload -- Local actions of natriuretic peptides and nitric oxide in cardiac remodelling: Implications for therapy -- Modulating G protein-coupled receptors to effect reverse cardiac remodeling -- Role of inflammation and matrix proteinases in cardiac remodeling following stress and injury -- Role of chymase in matrix and myocardial remodeling due to mitral regurgitation. Implications for therapy -- Cardiac remodeling due to aortic regurgitation and mitral regurgitation -- Reducing oxidative stress and manipulating molecular signaling events using resveratrol as a therapy for pathological cardiac hypertrophy -- Angiogenesis, arteriogenesis, and mitochondrial dysfunction -- Part II: Molecular mechanisms of remodeling after myocardial injury and infarction -- Subcellular remodeling and cardiac dysfunction due to ischemia-reperfusion injury -- Role of microRNAs in cardiac hypertrophy and post-infarction remodeling -- Negative regulators of inflammation as endogenous protective mechanisms in post-infarction remodeling -- TLR-dependent pathways and Akt/mTOR/P70S6K pathways in cardiac remodeling after myocardial infarction -- The STAT3 pathway and downstream mechanisms in cardiac remodeling: Friend or foe -- The role of growth differentiation factor 5 in cardiac repair post myocardial infarction -- Extracellular matrix biomarkers of adverse remodeling after myocardial infarction -- Oxidative stress in cardiac repair and remodeling: Molecular pathways and therapeutic strategies -- Role of SPARC in cardiac extracellular matrix remodeling after myocardial infarction -- Tissue inhibitor of matrix metalloproteinases in the pathogenesis of heart failure syndromes -- Intracellular matrix remodeling and cardiac function in ischemia-reperfusion injury -- Aging and markers of adverse remodeling after myocardial infarction -- Optimizing stem cell therapy for cardiac repair following a myocardial infarction -- Regulation of fibrosis after myocardial infarction. Implications for ventricular remodeling -- The ACE2/Ang-(1-7) pathway in cardiac fibroblasts as a potential target for cardiac remodeling.