Intro -- Preface -- Contents -- Part I: From Molecular Mechanism to Intervention for Congenital Heart Diseases, Now and the Future -- Perspective -- 1: Reprogramming Approaches to Cardiovascular Disease: From Developmental Biology to Regenerative Medicine -- 1.1 Introduction -- 1.2 Molecular Networks Regulate Cardiac Cell Fate -- 1.3 Cardiac Fibroblasts in the Normal and Remodeling Heart -- 1.4 Direct Cardiac Reprogramming In Vitro -- 1.5 Direct Cardiac Reprogramming In Vivo -- 1.6 Direct Cardiac Reprogramming in Human Fibroblasts -- 1.7 Challenges and Future Directions -- References -- 2: The Arterial Epicardium: A Developmental Approach to Cardiac Disease and Repair -- 2.1 Origin of the Epicardium -- 2.2 Epicardium-Derived Cells (EPDCs) -- 2.3 Heterogeneity of Epicardial Cells -- 2.3.1 The Cardiac Fibroblast -- 2.3.2 Arterial Smooth Muscle Cell -- 2.3.3 Endothelial Cells -- 2.3.4 Cardiomyocytes -- 2.3.5 The Purkinje Fiber -- 2.4 Congenital and Adult Cardiac Disease -- 2.4.1 Non-compaction -- 2.4.2 Conduction System Anomalies -- 2.4.3 Valvulopathies -- 2.4.4 Coronary Vascular Anomalies -- 2.5 Cardiovascular Repair -- 2.6 Future Directions and Clinical Applications -- References -- 3: Cell Sheet Tissue Engineering for Heart Failure -- 3.1 Introduction -- 3.2 Cell Sheet Engineering -- 3.3 Cardiac Tissue Reconstruction -- 3.4 Cell Sheet Transplantation in Small Animal Models -- 3.5 Cell Sheet Transplantation in Preclinical and Clinical Studies -- 3.6 Conclusions -- References -- 4: Future Treatment of Heart Failure Using Human iPSC-Derived Cardiomyocytes -- 4.1 Introduction -- 4.2 Cardiac Differentiation from Human iPSCs -- 4.3 Nongenetic Methods for Purifying Cardiomyocytes -- 4.4 Transplantation of Human PSC-Derived Cardiomyocytes -- 4.5 Future Directions -- References -- 5: Congenital Heart Disease: In Search of Remedial Etiologies.

5.1 Introduction -- 5.1.1 Emerging Concepts -- 5.1.2 Hub Hypothesis -- 5.2 Searching for Candidate Signaling Hubs in Heart Development -- 5.2.1 Nodal Signaling Kinases -- 5.2.2 Filamin A -- 5.2.3 Relevance of Signaling Hubs to CHD -- 5.3 Lineage Is a Key to Remedial Therapy -- 5.3.1 Postnatal Origin of Cardiac Fibroblasts -- 5.3.2 A Strategy to Use Fibroblast Progenitors to Carry Genetic Payloads -- 5.3.2.1 This Strategy Calls for a Conceptual Revision in Our Thinking About Fibroblasts -- 5.4 Remedial Therapies: Delivering Genetic ``Payloads�� -- 5.4.1 Preliminary Studies -- References -- Part II: Left-Right Axis and Heterotaxy Syndrome -- 6: Left-Right Asymmetry and Human Heterotaxy Syndrome -- 6.1 Introduction -- 6.2 Molecular and Cellular Mechanisms of Left-Right Determination -- 6.2.1 Node Cell Monocilia Create Leftward ``Nodal Flow�� and Activate Asymmetry Signaling Around the Node -- 6.2.2 Asymmetry Signaling Transmits to the Left Lateral Plate Mesoderm -- 6.2.3 Genes Associated with the Human Heterotaxy Syndrome -- 6.3 Clinical Manifestation of the Heterotaxy Syndrome -- 6.3.1 Right Isomerism -- 6.3.2 Left Isomerism -- 6.4 Long-Term Prognosis of Heterotaxy Patients -- 6.4.1 Protein-Losing Enteropathy -- 6.4.2 Arrhythmias -- 6.4.3 Heart Failure -- 6.4.4 Hepatic Dysfunction -- 6.4.5 Management of Failing Fontan Patients -- 6.5 Future Direction and Clinical Implications -- References -- 7: Roles of Motile and Immotile Cilia in Left-Right Symmetry Breaking -- 7.1 Introduction -- 7.2 Symmetry Breaking by Motile Cilia and Fluid Flow -- 7.3 Sensing of the Fluid Flow by Immotile Cilia -- 7.4 Readouts of the Flow -- 7.5 Future Directions -- References -- 8: Role of Cilia and Left-Right Patterning in Congenital Heart Disease -- 8.1 Introduction -- 8.1.1 Heterotaxy, Primary Ciliary Dyskinesia, and Motile Cilia Defects.

8.1.2 Motile Respiratory Cilia Defects in Other Ciliopathies -- 8.1.3 Ciliary Dysfunction in Congenital Heart Disease Patients with Heterotaxy -- 8.1.4 Respiratory Complications in Heterotaxy Patients with Ciliary Dysfunction -- 8.1.5 Left-Right Patterning and the Pathogenesis of Congenital Heart Disease -- 8.1.6 Ciliome Gene Enrichment Among Mutations Causing Congenital Heart Disease -- 8.1.7 Ciliary Dysfunction in Congenital Heart Disease Patients Without Heterotaxy -- 8.1.8 Future Directions and Clinical Implications -- References -- 9: Pulmonary Arterial Hypertension in Patients with Heterotaxy/Polysplenia Syndrome -- References -- Perspective -- Part III: Cardiomyocyte and Myocardial Development -- 10: Single-Cell Expression Analyses of Embryonic Cardiac Progenitor Cells -- 10.1 Introduction -- 10.2 CPCs of the Two Heart Fields -- 10.3 CPC Specification -- 10.4 The Potential of Single-Cell Transcriptomics in the Study of CPC Specification -- 10.5 Future Direction and Clinical Implication -- References -- 11: Meis1 Regulates Postnatal Cardiomyocyte Cell Cycle Arrest -- 11.1 Introduction -- 11.2 Results -- 11.2.1 Expression of Meis1 During Neonatal Heart Development and Regeneration -- 11.2.2 Cardiomyocyte Proliferation Beyond Postnatal Day 7 Following Meis1 Deletion -- 11.2.3 MI in Meis1 Overexpressing Heart Limits Neonatal Heart Regeneration -- 11.2.4 Regulation of Cyclin-Dependent Kinase Inhibitors by Meis1 -- 11.3 Future Direction and Clinical Implications -- References -- 12: Intercellular Signaling in Cardiac Development and Disease: The NOTCH pathway -- 12.1 Introduction -- 12.2 Left Ventricular Non-compaction (LVNC) -- 12.3 The NOTCH Signaling Pathway -- 12.4 NOTCH in Ventricular Chamber Development -- 12.5 Future Directions and Clinical Implications -- References.

13: The Epicardium in Ventricular Septation During Evolution and Development -- 13.1 Introduction -- 13.2 Septum Components in the Completely Septated Heart -- 13.3 The Presence of the Epicardium in Amniotes -- 13.4 The Epicardium in the Avian Heart -- 13.5 Disturbance of the Epicardium -- 13.6 Septum Components in Reptilian Hearts -- 13.7 Tbx5 Expression Patterns -- 13.8 Discussion -- References -- 14: S1P-S1p2 Signaling in Cardiac Precursor Cells Migration -- References -- 15: Myogenic Progenitor Cell Differentiation Is Dependent on Modulation of Mitochondrial Biogenesis through Autophagy -- 16: The Role of the Thyroid in the Developing Heart -- References -- Perspective -- Part IV: Valve Development and Diseases -- 17: Atrioventricular Valve Abnormalities: From Molecular Mechanisms Underlying Morphogenesis to Clinical Perspective -- 17.1 Introduction -- 17.2 RV-TV Dysplastic Syndrome -- 17.2.1 Anatomic Features of the Heart in Ebstein�s Anomaly Patients -- 17.2.2 Morphogenetic Features of the Heart in Patients with Uhl�s Anomaly -- 17.2.3 Absence of the TV -- 17.3 Bone Morphogenetic Proteins (BMPs) and Their Important Role in Cushion Formation -- 17.3.1 Role of BMP2 in Cushion Mesenchymal Cell (CMC) Migration -- 17.3.2 BMP2 Induces CMC Migration and Id and Twist Expression -- 17.3.3 BMP2 Induces Expression of ECM Proteins in the Post-EMT Cushion -- 17.4 The Role of BMP2 for Cardiomyocytes Formation -- 17.5 Future Direction -- References -- 18: Molecular Mechanisms of Heart Valve Development and Disease -- 18.1 Introduction -- 18.2 Heart Valve Development -- 18.3 Heart Valve Disease -- 18.3.1 Calcific Aortic Valve Disease (CAVD) -- 18.3.2 Myxomatous Valve Disease -- 18.4 Signaling Pathways in Heart Valve Development and Disease -- 18.5 Future Directions and Clinical Implications -- References.

19: A Novel Role for Endocardium in Perinatal Valve Development: Lessons Learned from Tissue-Specific Gene Deletion of the Tie... -- 19.1 Introduction -- 19.2 Model for Valvar Endocardial-Specific Gene Deletion -- 19.3 Tie1 Is Required for Late-Gestational and Early Postnatal Aortic Valve Remodeling -- 19.4 Future Directions -- References -- 20: The Role of the Epicardium in the Formation of the Cardiac Valves in the Mouse -- 20.1 Introduction -- 20.1.1 The AV Valves and Their Leaflets -- 20.1.2 The Epicardium and Epicardially Derived Cells (EPDCs) -- 20.1.3 The Contribution of EPDCs to the Developing AV Valves -- 20.2 The Role of Bmp Signaling in Regulating the Contribution of EPDC to the AV Valves -- 20.2.1 Epicardial-Specific Deletion of the Bmp Receptor BmpR1A/Alk3 Leads to Disruption of AV Junction Development -- 20.2.2 Discussion -- 20.2.3 Future Direction and Clinical Implications -- References -- 21: TMEM100: A Novel Intracellular Transmembrane Protein Essential for Vascular Development and Cardiac Morphogenesis -- References -- 22: The Role of Cell Autonomous Signaling by BMP in Endocardial Cushion Cells in AV Valvuloseptal Morphogenesis -- References -- Perspective -- Part V: The Second Heart Field and Outflow Tract -- 23: Properties of Cardiac Progenitor Cells in the Second Heart Field -- 23.1 Introduction -- 23.2 Demarcating the First and Second Heart Fields and Their Contributions to the Heart -- 23.3 New Insights into the Role and Regulation of Noncanonical Wnt Signaling in the Second Heart Field and the Origins of Cono... -- 23.4 Involvement of the Second Heart Field in Atrial and Atrioventricular Septal Defects -- 23.5 Future Directions and Clinical Implications -- References -- 24: Nodal Signaling and Congenital Heart Defects -- 24.1 Introduction -- 24.2 The Nodal Signaling Pathway -- 24.3 Requirement for Nodal in Development.

24.4 Congenital Heart Defects Associated with Perturbations in Nodal Signaling.

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Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, 2022. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries.