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Molecular Defects in Cardiovascular Disease provides an in-depth discussion of the molecular mechanisms underlying the genesis of cardiovascular defects and the implications this has on current and emerging targeted therapeutics.
Calcium overloading-induced oxidative stress-mediated cellular and subcellular remodeling.- Intracellular MMP-2: Role in normal and diseased hearts.- Control of the mesenchymal-derived cell phenotype by Ski and Meox2: A putative mechanism for post-developmental phenoconversion.- Elevated Na+/H+ exchanger expression and its role in myocardial disease.- Impact of perinatal chronic hypoxia on cardiac tolerance to acute ischemia.- Stem cell, microRNA and redox cycling.- Cardiac cell therapy: Present and future.- Macroscopic and microscopic aspects of cardiac dysfunction in congestive heart failure.- Cardiac dysfunction and metabolism: Unravelling the molecular cross-talk.- Metabolic remodeling of the hypertrophied heart.- Mechanisms for the regulation of phospholipase C gene expression in cardiac hypertrophy.- Molecular changes in fatty acid oxidation in the failing heart.- Cardiolipin metabolism in experimental and human heart failure.- Mechanisms underlying development of cardiomyocyte hypertrophy via Na-H exchange stimulation.- The structural basis of cardiac dysfunction in human heart failure.- Hormonal mechanisms of cardiac remodeling in heart failure.- Modulators of remodeling after myocardial infarction.- Phosphodiesterase-5 inhibitors in protection against doxorubicin-induced cardiomyopathy.- Molecular basis of pulmonary hypertension in left heart failure.- Modulation of Gi protein expression in hypertension: Molecular mechanisms.- Vascular dysfunction in heart disease.- Cellular and molecular mechanisms associated with salicylate inhibition of intimal hyperplasia balloon catheter-induced vascular injury.- Involvement of growth factor receptor and non receptor protein tyrosine kinases in endothelin 1 and angiotensin II-induced signaling pathways in the cardiovascular system.- Sarco/endoplasmic reticulum Ca2+ pump damage by oxidative stress: Implications forCa2+ entry.- Obesity-hypertension: Leptin as the common link to cardiovascular and renal dysregulation.- Cardiorenal protection in diabetes mellitus.- Molecular mechanisms in the pathogenesis of diabetic cardiomyopathy.