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Vascular Mechanobiology in Physiology and Disease (Cardiac and Vascular Biology, 8)

معرفی کتاب «Vascular Mechanobiology in Physiology and Disease (Cardiac and Vascular Biology, 8)» نوشتهٔ Markus Hecker (editor), Dirk J. Duncker (editor)، منتشرشده توسط نشر Springer International Publishing AG در سال 2021. این کتاب در 9 صفحه، فرمت pdf، زبان انگلیسی ارائه شده است.

This volume of the series Cardiac and Vascular Biology presents the most relevant aspects of vascular mechanobiology along with many more facets of this fascinating, timely and clinically highly relevant field. Mechanotransduction, mechanosensing, fluid shear stress, hameodynamics and cell fate, are just a few topics to name. All important aspects of vascular mechanobiology in health and disease are reviewed by some of the top experts in the field. This volume, together with a second title on cardiac mechanobiology featured in this series, will be of high relevance to scientists and clinical researchers in the area of vascular biology, cardiology and biomedical engineering. Preface Contents Contributors 1: Hemodynamics and Vascular Remodeling 1.1 Introduction 1.2 Mechanical Stress in Materials 1.3 Conditions for Equilibrium of Mechanical Stress 1.4 Hemodynamics 1.4.1 Flow in a Cylindrical Tube 1.4.2 Bulk Viscosity of Blood 1.4.3 Viscosity of Blood in Microvessels 1.4.4 The Reynolds Number 1.4.5 Flow at Low Reynolds Number 1.4.6 Flow at High Reynolds Number 1.5 Functional Demands on the Vasculature 1.6 Role of Hemodynamic Signals in Vascular Remodeling 1.7 Conclusions and Translational Perspectives References 2: Contributions of Wall Stretch and Shear Stress to Vascular Regulation: Molecular Mechanisms of Homeostasis and Expansion 2.1 Introduction 2.1.1 Shear Stress 2.1.2 Wall Stretch 2.2 Mechanosensing 2.2.1 Receptor Tyrosine Kinases 2.2.2 Integrins 2.2.3 Ion Channels 2.2.4 G-Proteins and G-Protein-Coupled Receptors 2.2.5 NADPH Oxidases 2.2.6 Glycocalyx 2.3 Transcriptional and Functional Response 2.3.1 Krüppel-Like Factors 2 and 4 2.3.2 Nuclear Factor Erythroid 2-Like 2.3.3 Nuclear Factor Kappa Beta 2.3.4 Activator Protein 1 2.3.5 Hypoxia-Inducible Factor 1α 2.3.6 Zyxin 2.4 Mechanical Stimuli in Vascular Growth 2.4.1 Arteriogenesis 2.4.2 Angiogenesis 2.5 Conclusion References 3: Biomechanics in Small Artery Remodeling 3.1 Introduction 3.2 Small Artery Remodeling: An Ongoing and Ubiquitous Process 3.2.1 A Biomechanical Definition of Remodeling 3.2.2 Remodeling as Part of Normal Homeostasis 3.2.3 Assessment of Small Artery Remodeling 3.2.4 Involvement of Remodeling in Pathology 3.2.4.1 Hypertension 3.2.4.2 Atherosclerosis 3.2.4.3 Obesity, Insulin Resistance and Diabetes Type 2 3.3 Current Evidence for Involvement of Wall Shear Stress Sensing 3.3.1 Role of WSS in Normal Homeostasis 3.3.1.1 Regulation of WSS 3.3.1.2 Mechanisms of WSS Sensing 3.3.2 Role of WSS in Pathological Remodeling 3.3.2.1 Intracranial Aneurysms 3.3.2.2 Altered Shear Sensitivity in Small Arteries 3.3.2.3 Arteriogenesis 3.4 Current Evidence for Involvement of Pressure and Wall Stress 3.4.1 Role of Wall Stress in Normal Homeostasis 3.4.1.1 Acute Regulation of Wall Stress 3.4.1.2 Structural Regulation of Wall Stress 3.5 Need for an Integrative Understanding of Remodeling 3.6 Conclusion References 4: New Kids on the Block: The Emerging Role of YAP/TAZ in Vascular Cell Mechanotransduction 4.1 Introduction 4.2 An Overview of the Hippo Signaling Pathway 4.3 Why Study YAP and TAZ in Mechanically Challenged Arteries: Arguments from Public DATA Repositories 4.4 The Vascular Wall and Its Mechanical Forces 4.5 Mechanoactivation of YAP and TAZ 4.6 Role of YAP and TAZ in the Formation of Blood Vessels 4.7 Shear Stress-Dependent Control of YAP and TAZ in Endothelial Cells 4.8 YAP and TAZ in Growth and Differentiation of Arterial SMCs 4.9 YAP and TAZ Contribute to Pulmonary Arterial Hypertension 4.10 YAP and TAZ in Aneurysmal Disease 4.11 YAP and TAZ Target Genes in the Mature Vascular Wall 4.12 Cross Talk Between YAP/TAZ and MRTFs 4.13 Clinical Translation References 5: GPCRs Under Flow and Pressure 5.1 Introduction 5.2 Mechanosensitive Proteins Discussed as Mechanosensors in Blood Vessels 5.3 Mechanosensitive GPCRs Essentially Contribute to Vascular Mechanosensing 5.4 Agonist and Mechanical Stimulation Induce Distinct Active Receptor Conformations 5.5 Helix 8 Is the Essential Structural Element Conferring GPCRs with Mechanosensitivity 5.6 Conclusion References 6: Hemodynamic Control of Endothelial Cell Fates in Development 6.1 Introduction 6.2 Hemodynamics in Vascular Development 6.2.1 The Vasculature at the Onset of Flow 6.2.2 Flow Induces Differentiation of Hierarchical Vasculature 6.2.3 Endothelial Cell Orientation and Active Vessel Regression 6.2.4 Flow Shapes the Aortic Arch 6.3 Mechanosensors: Structures for Detecting Shear Stress 6.3.1 Ion Channels 6.3.2 GPCRs 6.3.3 Integrins 6.3.4 The Glycocalyx 6.3.5 Primary Cilia 6.3.6 The Junctional Mechanosensory Complex 6.3.7 Caveolae 6.3.8 Shear Stress-Induced Gene Regulation for Arteriovenous and Lymphatic Differentiation 6.3.9 Notch Signaling 6.3.10 ALK1/Endoglin and ALK5 6.3.11 PROX1/FOXC2/GATA2 6.3.12 YAP and TAZ 6.3.13 Wnt/β-Catenin Signaling 6.3.14 TIE and ANG 6.3.15 KLF2 6.3.16 Coup-TFII 6.4 Specific Examples of Endothelial Differentiation Based on Flow Mechanics 6.4.1 Shear Stress and Endothelial Cell Sprouting 6.4.2 Shear Stress Governs Intussusception 6.4.3 Vascular Fusion is a Flow-Driven Process 6.4.4 Plasticity in Arteriovenous Identity 6.4.5 Altered Flow Reprograms Lymphatic Vessels to Blood Vessels 6.4.6 Oscillatory Flow in Valve Formation 6.5 Conclusion References 7: The Biomechanics of Venous Remodeling 7.1 Introduction 7.2 Anatomy and Physiology of the Venous System 7.2.1 Overview of the Cardiovascular System and Characterization of Blood Vessels 7.2.2 The Venous System, Structure and Function 7.3 Morphological and Functional Features of Varicose and Insufficient Veins 7.4 Risk Factors of Varicose Vein Development and Venous Insufficiency 7.5 Flow and Pressure in Healthy and Insufficient Veins 7.6 Biomechanically Evoked Venous Remodeling in Experimental Models 7.7 Mechanisms of Biomechanically Induced Venous Remodeling 7.8 Conclusions References 8: Mechanobiology of Lymphatic Vessels 8.1 Introduction 8.2 Expansion and Maturation of Lymphatic Vessels 8.2.1 Interstitial Forces 8.2.2 Luminal Shear Stress 8.3 Postnatal Lymphangiogenesis 8.3.1 Interstitial Flow 8.3.2 Shear Stress 8.4 Trans-Endothelial Transport 8.5 Lymphatic Contractility 8.5.1 Luminal Shear Stress 8.5.2 Transmural Pressure 8.5.3 Nervous Stimulation 8.6 Lymphatic Vasculature in Disease 8.6.1 Contractile Dysfunction 8.6.2 Lymphangiogenesis 8.6.3 Collecting Lymphatic Malformation and Remodeling 8.7 Chapter Summary References 9: Mechanical Regulation of Epigenetic Modifications in Vascular Biology and Pathobiology 9.1 Introduction 9.2 Vascular Mechanobiology 9.2.1 Shear Stress 9.2.1.1 Shear Stress Modulates Vascular Morphogenesis 9.2.1.2 Shear Stress Regulates Physiological Functions 9.2.1.3 Shear Stress Is Involved in the Development of Vascular Pathologies 9.2.2 Stretch Force 9.2.2.1 Cyclic Stretch Regulates Physiological Functions in Vascular SMCs and ECs 9.2.2.2 Cyclic Stretch Regulates Pathophysiological Changes in Vascular SMCs and ECs 9.3 Epigenetics 9.3.1 Methylation 9.3.2 Histone Modification and Chromatin Remodeling 9.3.3 RNA-Based Mechanisms 9.4 Mechanical Force-Induced Epigenetic Modifications in Vascular Health and Disease 9.4.1 Methylation 9.4.2 Histone Modification 9.4.2.1 Class I HDACs 9.4.2.2 Class II HDACs 9.4.2.3 Class III HDACs 9.4.3 MicroRNA 9.4.3.1 miRNAs Are Regulated by Shear Stress 9.4.3.2 miRNAs Are Regulated by Cyclic Stretch 9.4.3.3 Extracellular miRNAs 9.4.4 Long Noncoding RNA 9.5 Conclusions and Future Perspectives References 10: Mechanobiology of Arterial Hypertension 10.1 Introduction 10.2 Mechanical Force Exerts Stress That Creates Tension in the Tissue 10.3 Vascular Adaptations in Small Arteries to Enhanced Wall Tension During Hypertension 10.3.1 Acute Response: Myogenic Constriction 10.3.2 Chronic Adaptations: Vascular Remodeling 10.4 Structural and Mechanical Alterations in Large Arteries in Hypertension 10.5 Large Artery Stiffness and Pulse Wave Velocity 10.6 Functional Consequences of the Change in Effective Distensibility References 11: Mechanosensing and Mechanotransduction in Pulmonary Hypertension 11.1 Introduction 11.2 Changes in Mechanical Characteristics of the Pulmonary Vasculature in PH 11.3 Changes in Mechanical Forces Acting on the Pulmonary Vasculature in PH 11.4 Impact of Altered Mechanical Forces on Pulmonary Vasculature 11.4.1 Altered Mechanotransduction in Pulmonary Endothelial Cells 11.4.2 Altered Mechanotransduction in Pulmonary Vascular Smooth Muscle Cells 11.4.3 Mechano-metabolic Coupling 11.4.4 Mechanosensors 11.4.4.1 Caveolae 11.4.4.2 Mechanosensitive Ion Channels 11.4.4.3 Integrins and Cytoskeleton 11.4.5 Mechanotransduction: Transcriptional Regulation 11.5 Role of Extracellular Matrix 11.6 Conclusions and Perspectives References 12: Mechanobiology of Atherosclerosis 12.1 Introduction 12.2 The Endothelial Glycocalyx is an Amplifying Mechanosensor 12.3 Mechano-redox Regulation of Antioxidant Enzymes 12.4 Mechanical Force-Induced CD40 Signaling Results in Endothelial Dysfunction 12.5 Mechanosensitive Transcription Factors 12.6 Flow-Induced Epigenetic Mechanisms of Endothelial Gene Expression 12.7 Conclusions and Remaining Questions References 13: Exploitation of Vascular Mechanobiology for Therapy Innovations 13.1 Introduction 13.2 Mechanobiological Foundations for Therapeutic Innovations 13.3 Mechanobiology-Driven Innovations in Cardiovascular Therapy 13.3.1 Vascular Stent 13.3.2 Vascular Graft 13.3.3 Regenerative Medicine 13.3.4 Medications 13.3.5 Disease Management 13.4 Vascular Mechanomedicine: Perspectives and Challenges References
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