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Cardiac Fibrosis and Heart Failure Cause or Effect 1st edition by lan Dixon, Jeffrey Wigle ISBN 3319174372 9783319174372

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ISBN 10: 3319174372
ISBN 13: 9783319174372
Author: lan Dixon, Jeffrey Wigle

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.

Cardiac Fibrosis and Heart Failure Cause or Effect 1st Table of contents:

1. Introduction

2. Cardiac Fibroblasts in Normal Mammalian Hearts

3. The Phases of Cardiac Repair

4. Cardiac Fibroblasts During the Inflammatory Phase

  • 4.1 Cardiac Fibroblasts as Inflammatory Cells Following an Ischemic Insult

  • 4.2 Do Activated Fibroblasts Participate in Resolution of Post-Infarction Inflammation?

5. Cardiac Fibroblasts During the Proliferative Phase

  • 5.1 Activated Fibroblasts as the Dominant Reparative Cells in the Infarcted Myocardium

  • 5.2 Characteristics and Origin of Activated Fibroblasts Following Infarction

  • 5.3 Myofibroblast Transdifferentiation

  • 5.4 Role of TGF-β Signaling and Its Importance in Fibrosis

  • 5.5 Signals Regulating Fibroblast Migration in the Infarcted Myocardium

  • 5.6 The Renin-Angiotensin-Aldosterone System (RAAS) and Growth Factors Regulate Fibroblast Function

  • 5.7 The Extracellular Matrix as a Modulator of Fibroblast Phenotype: The Matricellular Proteins

6. Cardiac Fibroblasts During the Maturation Phase of Infarct Healing

7. Cardiac Fibroblasts in the Remodeling Non-Infarcted Heart

8. Therapeutic Opportunities: Targeting the Cardiac Fibroblast Following Myocardial Infarction

9. Conclusions

10. References

Chapters on Specialized Topics

Mechanical and Matrix Regulation of Valvular Fibrosis

  • 1 Introduction

    • 1.1 Aortic Valve Biology, Physiology, and Function

    • 1.2 Aortic Valve Fibrosis

  • 2 Fibrosis, Biomechanics and the Myofibroblast

  • 3 TGF-β-Mediated Mechanotransduction of Valvular Myofibrogenesis

  • 4 Mechanical Control of Valvular Myofibroblast Differentiation Independent of TGF-β

  • 5 Impact of Aortic Valve Disease and Biomechanics on Cardiac Fibrosis

  • 6 Conclusions

  • References

Bone Marrow-Derived Progenitor Cells, micro-RNA, and Fibrosis

  • 1 Introduction

  • 2 Cell Sources of Fibrosis

    • 2.1 Mesenchymal Progenitor Cells (MPCs)

    • 2.2 Fibrocytes

    • 2.3 Other Differentiating Cell Sources

  • 3 Influence of miRNA on Cell Differentiation and Fibrosis

  • 4 Conclusions

  • References

The Stressful Life of Cardiac Myofibroblasts

  • 1 Introduction

  • 2 A Myofibroblast Is a Myofibroblast, Of Course?

    • 2.1 Myofibroblast Features

    • 2.2 Cardiac Myofibroblast Precursors

  • 3 More than Just Material for Myofibroblasts: The ECM of the Heart

    • 3.1 Composition and Function of the ECM

    • 3.2 ECM Mechanics and Myofibroblast Activation

  • 4 TGF-β1 at the Crossroads of ECM and Growth Factor Signaling

  • 5 ECM Receptors in Cardiac Myofibroblast Differentiation

  • 6 Conclusions

  • References

Pathogenic Origins of Fibrosis in Hypertensive Heart Disease

  • 1 Introduction

  • 2 Hypertensive Heart Disease

    • 2.1 Human HHD

    • 2.2 Animal Model of HHD

    • 2.3 Remodeling Independent of Hypertension

  • 3 Cardiac Myocyte Necrosis as Pathogenic Origin to Microscopic Scarring

    • 3.1 Prooxidant Pathway

    • 3.2 Antioxidant Pathways in Cardioprotection

  • 4 Immunostimulatory State and Perivascular Fibrosis

    • 4.1 Proinflammatory Vascular Phenotype

    • 4.2 Induction of Oxidative Stress

    • 4.3 Cardioprotection

  • 5 Myofibroblasts and Cardiac Fibrosis

  • 6 Summary and Conclusions

  • References

Embryological Origin of Valve Progenitor Cells

  • 1 Introduction

  • 2 Early Cardiogenesis and Valve Progenitor Specification

    • 2.1 Overview of Cardiac Development

    • 2.2 Endocardium Formation

    • 2.3 Epicardium

    • 2.4 Neural Crest

  • 3 Valve Maturation

  • 4 Valvulopathies, Cardiac Fibrosis, and Aortic Stenosis

  • 5 Conclusions

  • References

Diverse Cellular Origins of Cardiac Fibroblasts

  • 1 Introduction

  • 2 Phenotypes

    • 2.1 Fibroblasts

    • 2.2 Protomyofibroblasts

    • 2.3 Myofibroblasts

  • 3 Origins During Development

  • 4 Sources of Fibroblasts in Pathology

  • 5 Resident Fibroblasts

  • 6 Epithelial to Mesenchymal Transition (EMT)

  • 7 EMT-Derived Fibroblasts in Cardiac Disease

  • 8 Endothelial to Mesenchymal Transition (EndMT)

  • 9 Bone Marrow-Derived Progenitor Cells

  • 10 Monocytes

  • 11 Fibrocytes

  • 12 Perivascular Cells

  • 13 Importance of Understanding Fibroblast Origins

  • References

Non-Canonical Regulation of TGF-β1 Signaling

  • 1 TGF-β Signaling

  • 2 TGF-β1 and Mechanical Stress

  • 3 Ski/Sno Superfamily

  • 4 Regulation of Ski/Sno by TGF-β

  • 5 Ski/Sno Regulation of TGF-β1

  • 6 Ski/Sno in Cardiac Fibrosis

  • 7 Hippo Pathway

  • 8 YAP/TAZ and Mechanical Stress

  • 9 Cross-Talk Between Hippo and TGF-β Pathways

  • 10 YAP Effects in the Heart

  • 11 Synopsis

  • References

Index

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Tags: lan Dixon, Jeffrey Wigle, Cardiac Fibrosis, Heart Failure