Cardiac Fibrosis and Heart Failure: Cause or Effect? (Advances in Biochemistry in Health and Disease Book 13)

The unique biology of cardiac fibroblasts and related cells, such as cardiac myofibroblasts and valvular interstitial cells, distinguish them from other fibroblastic cells, a concept that is only beginning to be widely appreciated. Further, the natural signals that stimulate and inhibit cardiac fibrosis within these cells are not well understood. This volume compiles articles that address the molecular mechanisms that control the synthesis and secretion of the cardiac ECM. The book showcases chapters that highlight discussion of role of Transforming Growth Factor β (TGFβ), an important fibrogenic cytokine, and its downstream effectors SMAD in many cardiac diseases. Further, the contributions highlight information to discuss endogenous inhibitors of cardiac fibrosis, as well as advances in tissue engineering specific to matrix in the heart. Finally, discussions of unifying mechanisms of matrix remodeling in valves and myocardium are presented. The mechanisms involved in the stimulation of cardiac fibrosis are not fully understood. In most cases the marginal attenuation of cardiac fibrosis as a result of a given therapy is a beneficial side-effect linked to other primary effects on other cells, especially cardiomyocytes. Very few drugs or agents are known to affect the function and dysfunction of cardiac fibroblasts and myofibroblasts alone. The book helps to translate the information gathered within to allow us to alter the course of fibrogenic events that are typical of cardiac fibrosis, and thereby reduce their burden on the patient and on society itself Front Matter....Pages i-xv Cardiac Fibrosis and Heart Failure—Cause or Effect?....Pages 1-4 Fibroblast Activation in the Infarcted Myocardium....Pages 5-22 Mechanical and Matrix Regulation of Valvular Fibrosis....Pages 23-53 Bone Marrow-Derived Progenitor Cells, micro-RNA, and Fibrosis....Pages 55-69 The Stressful Life of Cardiac Myofibroblasts....Pages 71-92 Pathogenic Origins of Fibrosis in the Hypertensive Heart Disease that Accompanies Aldosteronism....Pages 93-107 Embryological Origin of Valve Progenitor Cells....Pages 109-123 Diverse Cellular Origins of Cardiac Fibroblasts....Pages 125-145 Non-Canonical Regulation of TGF-β1 Signaling: A Role for Ski/Sno and YAP/TAZ....Pages 147-165 Molecular Mechanisms of Smooth Muscle and Fibroblast Phenotype Conversions in the Failing Heart....Pages 167-179 Current and Future Strategies for the Diagnosis and Treatment of Cardiac Fibrosis....Pages 181-217 Remodelling of the Cardiac Extracellular Matrix: Role of Collagen Degradation and Accumulation in Pathogenesis of Heart Failure....Pages 219-235 Matrix Metalloproteinase 9 (MMP-9)....Pages 237-259 Collagen Processing and its Role in Fibrosis....Pages 261-278 Mechanisms of Cardiac Fibrosis and Heart Failure....Pages 279-297 Mathematical Simulations of Sphingosine-1-Phosphate Actions on Mammalian Ventricular Myofibroblasts and Myocytes....Pages 299-322 Extracellular Matrix and Cardiac Disease: Surgical and Scientific Perspectives....Pages 323-346 The Role of Neurohumoral Activation in Cardiac Fibrosis and Heart Failure....Pages 347-381 Natriuretic Peptides: Critical Regulators of Cardiac Fibroblasts and the Extracellular Matrix in the Heart....Pages 383-404 Cardiac Tissue Engineering for the Treatment of Heart Failure Post-Infarction....Pages 405-418 Mechanisms of Cardiac Valve Failure and the Development of Tissue Engineered Heart Valves....Pages 419-431 Back Matter....Pages 433-436 The unique biology of cardiac fibroblasts and related cells, such as cardiac myofibroblasts and valvular interstitial cells, distinguish them from other fibroblastic cells, a concept that is only beginning to be widely appreciated.℗l Further, the natural signals that stimulate and inhibit cardiac fibrosis within these cells are not well understood.℗l This volume compiles articles that address the molecular mechanisms that control the synthesis and secretion of the cardiac ECM.℗l℗l The book showcases chapters that highlight discussion of role of Transforming Growth Factor lø (TGFlø), an important fibrogenic cytokine, and its downstream effectors SMAD in many cardiac diseases. Further, the contributions highlight information to discuss endogenous inhibitors of cardiac fibrosis, as well as advances in tissue engineering specific to matrix in the heart. Finally, discussions of unifying mechanisms of matrix remodeling in valves and myocardium are presented.℗l The mechanisms involved in the stimulation of cardiac fibrosis are not fully understood.℗l In most cases the marginal attenuation of cardiac fibrosis as a result of a given therapy is a beneficial side-effect linked to other primary effects on other cells, especially cardiomyocytes.℗l Very few drugs or agents are known to affect the function and dysfunction of cardiac fibroblasts and myofibroblasts alone.℗l The book helps to translate the information gathered within to allow us to alter the course of fibrogenic events that are typical of cardiac fibrosis, and thereby reduce their burden on the patient and on society itself