Kooperativer Bibliotheksverbund

UID:

Format: 1 Online-Ressource (XVIII, 527 p. 83 illus., 59 illus. in color)

Edition: 1st ed. 2022

ISBN: 9783031083099

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08308-2

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08310-5

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08311-2

Language: English

DOI: 10.1007/978-3-031-08309-9

URL: Volltext  (URL des Erstveröffentlichers)

UID:

Format: 1 Online-Ressource(XVIII, 527 p. 83 illus., 59 illus. in color.)

Edition: 1st ed. 2022.

ISBN: 9783031083099

Content: Part 1: Cardiac Signaling -- Chapter 1: Calcium-Dependent Signaling in Cardiac Myocytes -- Chapter 2: Organization of Ca2+ Signaling Microdomains in Cardiac Myocytes -- Chapter 3: Stress Kinase Signaling in Cardiac Myocytes -- Chapter 4: Cardiotoxicity and cardiac cell signaling -- Chapter 5: Protein Phosphatase Signaling in Cardiac Myocytes -- Chapter 6: Metabolic Regulation of Mitochondrial Dynamics and Cardiac Function -- Chapter 7: NADPH Oxidase System Mediates Cholesterol Secoaldehyde-Induced Oxidative Stress and Cytotoxicity in H9c2 Cardiomyocytes -- Chapter 8: Lipid Mediators in Cardiovascular Physiology and Disease -- Chapter 9: Cardiac Inflammasome and Arrhythmia -- Chapter 10: Myocardial Fibrosis: Cell Signaling and In Vitro Modeling -- Chapter 11: Neural regulation of cardiac rhythm -- Part 2: Vascular Signaling -- Chapter 12: Mechanisms of lipoproteins and reverse cholesterol transport in atherosclerotic cardiovascular disease -- Chapter 13: Atherosclerotic plaque regression: Future perspective -- Chapter 14: Role of Bioactive Lipid, Phosphatidic Acid in Hypercholesterolemia Drug-induced Myotoxicity – Statin-induced Phospholipase D (PLD) Lipid Signaling in Skeletal Muscle Cells -- Chapter 15: Cell-Cell Communication in the Vascular Endothelium -- Chapter 16: Lysophosphatidic acid regulates endothelial barrier integrity -- Chapter 17: Regulation of Vascular Endothelial Barrier Integrity and Function by Lipid-Derived Mediators -- Chapter 18: Hyperglycemic Oxoaldehyde (Glyoxal)-induced Vascular Endothelial Cell Damage through Oxidative Stress is protected by Thiol Iron Chelator, Dimercaptosuccinic Acid – Role of Iron in Diabetic Vascular Endothelial Dysfunction.

Content: This contributed volume focuses on cardiovascular diseases (CVDs), and explores the ways in which signaling mechanisms at the biochemical, molecular, and cellular levels in the blood vessels (vascular) and heart contribute to the underlying causes of development and progression of the CVDs. This volume covers unique topics such as oxidant signaling in vascular and heart diseases and health, cytoskeletal signaling in vascular health and disease, phospholipase signaling in CVDs, lipid signaling in vascular and myocardial health and diseases, and drug discovery in cellular signaling for cardiovascular diseases. This book assembles the most important discoveries made by leaders on the cellular signaling mechanisms operating behind the development and progression of life-threatening CVDs. It is an extremely useful resource for the investigators in the field of CVDs, and opens the discussion for further discovery of efficient management and effective treatment of the CVDs.

Additional Edition: ISBN 9783031083082

Additional Edition: ISBN 9783031083105

Additional Edition: ISBN 9783031083112

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 9783031083082

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 9783031083105

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 9783031083112

Language: English

DOI: 10.1007/978-3-031-08309-9

URL: lizenzpflichtig

UID:

Format: XVIII, 527 p. 83 illus., 59 illus. in color. , online resource.

Edition: 1st ed. 2022.

ISBN: 9783031083099

Content: This contributed volume focuses on cardiovascular diseases (CVDs), and explores the ways in which signaling mechanisms at the biochemical, molecular, and cellular levels in the blood vessels (vascular) and heart contribute to the underlying causes of development and progression of the CVDs. This volume covers unique topics such as oxidant signaling in vascular and heart diseases and health, cytoskeletal signaling in vascular health and disease, phospholipase signaling in CVDs, lipid signaling in vascular and myocardial health and diseases, and drug discovery in cellular signaling for cardiovascular diseases. This book assembles the most important discoveries made by leaders on the cellular signaling mechanisms operating behind the development and progression of life-threatening CVDs. It is an extremely useful resource for the investigators in the field of CVDs, and opens the discussion for further discovery of efficient management and effective treatment of the CVDs.

Note: Part 1: Cardiac Signaling -- Chapter 1: Calcium-Dependent Signaling in Cardiac Myocytes -- Chapter 2: Organization of Ca2+ Signaling Microdomains in Cardiac Myocytes -- Chapter 3: Stress Kinase Signaling in Cardiac Myocytes -- Chapter 4: Cardiotoxicity and cardiac cell signaling -- Chapter 5: Protein Phosphatase Signaling in Cardiac Myocytes -- Chapter 6: Metabolic Regulation of Mitochondrial Dynamics and Cardiac Function -- Chapter 7: NADPH Oxidase System Mediates Cholesterol Secoaldehyde-Induced Oxidative Stress and Cytotoxicity in H9c2 Cardiomyocytes -- Chapter 8: Lipid Mediators in Cardiovascular Physiology and Disease -- Chapter 9: Cardiac Inflammasome and Arrhythmia -- Chapter 10: Myocardial Fibrosis: Cell Signaling and In Vitro Modeling -- Chapter 11: Neural regulation of cardiac rhythm -- Part 2: Vascular Signaling -- Chapter 12: Mechanisms of lipoproteins and reverse cholesterol transport in atherosclerotic cardiovascular disease -- Chapter 13: Atherosclerotic plaque regression: Future perspective -- Chapter 14: Role of Bioactive Lipid, Phosphatidic Acid in Hypercholesterolemia Drug-induced Myotoxicity - Statin-induced Phospholipase D (PLD) Lipid Signaling in Skeletal Muscle Cells -- Chapter 15: Cell-Cell Communication in the Vascular Endothelium -- Chapter 16: Lysophosphatidic acid regulates endothelial barrier integrity -- Chapter 17: Regulation of Vascular Endothelial Barrier Integrity and Function by Lipid-Derived Mediators -- Chapter 18: Hyperglycemic Oxoaldehyde (Glyoxal)-induced Vascular Endothelial Cell Damage through Oxidative Stress is protected by Thiol Iron Chelator, Dimercaptosuccinic Acid - Role of Iron in Diabetic Vascular Endothelial Dysfunction.

In: Springer Nature eBook

Additional Edition: Printed edition: ISBN 9783031083082

Additional Edition: Printed edition: ISBN 9783031083105

Additional Edition: Printed edition: ISBN 9783031083112

Language: English

DOI: 10.1007/978-3-031-08309-9

URL: https://doi.org/10.1007/978-3-031-08309-9

UID:

Format: 1 online resource (535 pages)

ISBN: 3-031-08309-1

Note: Intro -- Preface on the Current Trends in Cardiovascular Signaling in Health and Disease -- Calcium- and Stress-Dependent Signaling in Cardiac Myocytes -- Reactive Oxygen Species and Lipid Signaling in Cardiac Myocytes -- Inflammatory Signaling, Fibrosis, and Cardiac Function -- Neural Regulation of Cardiac Rhythm -- Reverse Cholesterol Transport in Atherosclerotic Cardiovascular Disease -- Progression of the Atherosclerotic Plaque Regression -- Role of Bioactive Lipid, Phosphatidic Acid in Statin-Induced Myotoxicity -- Cell-to-Cell Communication in the Vascular Endothelium -- The Bioactive Phospholipid, Lysophosphatidic Acid Regulates Vascular Endothelial Barrier Integrity -- Role of Lipid Mediators in Regulation of Vascular Endothelial Barrier Integrity and Function -- Role of Iron in Diabetic Vascular Endothelial Dysfunction -- Acknowledgments -- Contents -- Authors Biography -- Part I: Cardiac Signaling -- Calcium-Dependent Signaling in Cardiac Myocytes -- Introduction -- Physiology -- Pathophysiology -- Heart Failure -- Arrhythmias -- Ca-Dependent CaMKII Signaling in the Cardiac Myocyte -- Background -- Ca-Dependent CaMKII Signaling in Cardiac Myocyte Function and Disease -- CaMKII Structure and Ca-Dependent Activation -- Posttranslational Modifications of CaMKII as Novel Mechanisms of Cardiac Disease -- Cardiac Myocyte Remodeling and Ultrastructural Change -- Background -- Ultrastructural (T-Tubule) Remodeling -- RyR Remodeling -- Consequence of Structural Remodeling on Spatiotemporal Factors of Ca Release -- Potential Treatments -- Conclusions and Research Frontiers -- Spatial and Temporal Heterogeneity of Ca-Dependent Signaling -- Considerations for Therapy -- References -- Organization of Ca2+ Signaling Microdomains in Cardiac Myocytes -- Introduction -- Calcium Signaling in Cardiomyocytes. , Calcium Signaling Microdomains in Cardiomyocytes -- TT/jSR Microdomains in Systolic and Diastolic Calcium Handling -- Organization of cBIN1 and JP2 Microdomains at TT/jSR Membrane -- Calcium Signaling at the cBIN1 and Other TT/jSR Microdomains -- TT/jSR Microdomains, Calcium Signaling, and Heart Failure -- Ankyrin-Spectrin Microdomains in Calcium Signaling -- Organization of Ankyrin B-βII Spectrin Microdomains -- Ankyrin-Spectrin Microdomain-Regulated Calcium Signaling -- Ankyrin-Spectrin Microdomains in Cardiovascular Diseases -- Caveolae Microdomains in Calcium Signaling and Stress Response -- Organization of Caveolae Microdomains in Cardiomyocytes -- Caveolae-Related Organization of Calcium Signaling -- Caveolae, Calcium Signaling, and Disease -- Conclusions and Future Perspectives -- References -- Stress Kinase Signaling in Cardiac Myocytes -- Introduction -- Stress Kinase MAPK Signaling in the Heart -- JNK -- P38 -- ERK -- MAPKs and Calcium Homeostasis in Myocytes -- Normal and Abnormal Calcium (Ca2+) Signaling in Myocytes -- MAPKs in Stress-Evoked Ca2+ Mishandling in Myocytes -- MAPKs and Ca Handling Proteins in Myocytes -- MAPKs and Molecular Remodeling in Myocytes -- MAPKs and Gene Regulation in Myocytes -- MAPKs and Apoptotic Signaling Pathways in Stress-Exposed Myocytes -- JNK and Apoptotic Signaling Pathways in Myocytes -- p38 and Apoptotic Signaling Pathways in Myocytes -- ERK and Apoptotic Signaling Pathways in Myocytes -- Dynamic Relationships of MAPKs in Pathological Cardiac Remodeling in Stressed Hearts -- MAPKs and Therapeutic Potentials -- References -- Intracellular Cardiac Signaling Pathways Altered by Cancer Therapies -- Part I: Introduction -- Tyrosine Kinase Inhibitor Therapy -- Immune Checkpoint Therapy -- CAR T-Cell Therapy -- Part II: Tyrosine Kinases Inhibitor Therapy -- Tyrosine Kinase Signaling. , Abnormal Tyrosine Kinase Activity and Signaling in Cancer -- Tyrosine Kinase Inhibitors -- Tyrosine Kinase Receptors and Cardiomyopathy -- VEGF/VEGFR Signaling -- PDGF/ PDGFR Signaling -- c-KIT Signaling -- TKI-Induced Cardiovascular Dysfunction -- Hypertension -- Arrhythmias -- TKIs and Ion Homeostasis -- TKI-Mediated Potassium Ion Channel Dysfunction -- TKI Dysregulation of Calcium-Mediated Signaling -- TKIs and Sodium Channels: An Unexplored Territory -- TKIs and Heart Failure -- TKIs and Thromboembolism -- Monitoring and Treatment of TKI-Induced Cardiotoxicity -- Part III: Immune Checkpoint Inhibitors -- T-Cell Activation and Regulation -- Mechanisms of ICI-Mediated Cardiac Disorders -- Arrhythmias -- Myocarditis and Pericarditis -- Heart Failure -- Monitoring and Treatment of ICI-Associated Cardiotoxicity -- Part IV: CAR T-Cell Immunotherapy -- CAR T-Cell Mechanism of Action -- Proposed Mechanisms of Cardiotoxicity in CAR T-Cell Therapy -- JAK/STAT Signaling Pathway -- IL-6 -- TNFα -- Interleukin 1 -- Off-Target Affects -- Monitoring of CAR T-Cell Associated Cardiotoxicity -- Current and Proposed Treatments for CAR T-Cell-Induced Cardiotoxicity -- References -- Protein Phosphatase Signaling in Cardiac Myocytes -- Introduction -- The Kinase-Phosphatase Axis -- Protein Phosphatase Families and Genetics -- Localization and Binding Partners of Protein Phosphatases -- Mouse Models -- Protein Phosphatases in Cardiovascular Disease -- PP1 in Cardiovascular Disease -- PP2A in Cardiovascular Disease -- PP2B in Cardiovascular Disease -- Conclusions and Future Directions -- References -- Metabolic Regulation of Mitochondrial Dynamics and Cardiac Function -- Mitochondrial Dynamics: Fusion and Fission Events -- Diabetes-Related Cardiac Ischemia and Reperfusion Injury -- Diabetes-Related Cardiac Chronic Remodeling, Hypertrophy, and Failure. , Metabolic Control of Mitochondrial Dynamics: The Role of AMPK -- Concluding Remarks -- References -- NADPH Oxidase System Mediates Cholesterol Secoaldehyde-Induced Oxidative Stress and Cytotoxicity in H9c2 Cardiomyocytes -- Introduction -- Materials and Methods -- Chemicals, H9c2 Cardiomyocytes, and Cell Culture Supplies -- Synthesis of Cholesterol Secoaldehyde -- Cell Culture and Treatments -- Cell Proliferation and Metabolism -- Trypan Blue Exclusion Assay -- Measurement of Intracellular Peroxides -- Measurement of Hydrogen Peroxide -- Thiobarbituric Acid-Reactive Substances (TBARs) -- Measurement of Reduced Glutathione Levels -- Assay of Superoxide Dismutase Activity -- Measurement of Mitochondrial Transmembrane Potential -- Western Blot Analysis -- Statistical Analysis -- Results -- Apocynin Exacerbates While DPI Reduces the ChSeco-Induced Cytotoxic Response in H9c2 Cardiomyocytes -- NOS Inhibitors Attenuate the Formation of Peroxide or Peroxide-Like Substances in ChSeco-Exposed H9c2 Cardiomyocytes -- Apocynin Lowers the GSH Levels in ChSeco-Exposed Cardiomyocytes -- Apocynin But Not DPI Enhances the ChSeco-Induced Activation of SOD Activity in H9c2 Cardiomyocytes -- Apocynin and DPI Pretreatment in H9c2 Cardiomyocytes Reduces TBARs Formed in Response to the Exposure of ChSeco -- ChSeco-Induced Loss in Mitochondrial Transmembrane Potential Is Reversed by Pretreatments with Apocynin and DPI -- ChSeco-Induced Overexpression of pp38 and pSAPK in H9c2 Cardiomyocytes Is Mitigated by Pretreatments with Apo and DPI -- Discussion -- Conclusion -- References -- Lipid Mediators in Cardiovascular Physiology and Disease -- Introduction -- Lipid Mediators -- Oxylipins -- PUFA Reservoirs -- Oxylipin Synthesis -- Cyclooxygenase-Derived Oxylipins -- Lipoxygenase-Derived Oxylipins -- Cytochrome P450-Derived Oxylipins -- Conclusion and Future Perspectives. , References -- Cardiac Inflammasome and Arrhythmia -- Introduction -- Cardiac Electrophysiology -- Pathophysiology of AF -- Inflammasome Signaling -- Cardiac Inflammasome Signaling and Arrhythmogenesis -- Inflammasome-Mediated Pathogenesis of AF -- Nlrp3 Inflammasome Links AF Risk Factors to Atrial Arrhythmogenesis -- Nodal Signaling Points of Nlrp3 Activation -- Therapeutic Potential of Targeting the Cardiac NLRP3 Inflammasome -- Summary and Future Perspectives -- References -- Myocardial Fibrosis: Cell Signaling and In Vitro Modeling -- Introduction -- The Normal Myocardium -- Myocardial Fibrosis -- Modeling Myocardial Fibrosis -- Mechanotransduction -- Cell-Cell and Cell-ECM Interactions -- Pro-Fibrotic Soluble Mediators -- Conclusion -- References -- Neural Regulation of Cardiac Rhythm -- Introduction -- Neuronal Anatomy and Organization -- Cardiac Responses to Neurochemicals -- Adrenergic Signaling -- Muscarinic Signaling -- Co-transmission -- In vitro Models to Study Neural Regulation of Cardiac Rhythm -- Co-cultures -- Isolated Heart and Tissue Preparations -- Conclusions -- References -- Part II: Vascular Signaling -- Mechanisms of Lipoproteins and Reverse Cholesterol Transport in Atherosclerotic Cardiovascular Disease -- Introduction -- Lipoproteins Involved in Cholesterol Transport -- The Reverse Cholesterol Transport Pathway -- Mechanisms of Diseases Associated with Atherosclerotic CVD -- Genetic Predisposition to Cholesterol-Driven Cardiovascular Disease -- Therapeutic Approaches Targeting Lipoproteins -- LDL-C-Targeted Therapies -- HDL-C-Targeted Therapies -- References -- Atherosclerotic Plaque Regression: Future Perspective -- Introduction -- Development of Atherosclerotic Plaque and Formation of Primary Oxidation Products -- Role of Protein Carbonyls in Atherosclerotic Plaque Progression -- Factors Affecting Plaque Regression. , Increasing HDL Cholesterol.

Additional Edition: Print version: Parinandi, Narasimham L. Cardiovascular Signaling in Health and Disease Cham : Springer International Publishing AG,c2022 ISBN 9783031083082

Language: English

Keywords: Llibres electrònics

UID:

Format: 1 online resource (535 pages)

ISBN: 3-031-08309-1

Note: Intro -- Preface on the Current Trends in Cardiovascular Signaling in Health and Disease -- Calcium- and Stress-Dependent Signaling in Cardiac Myocytes -- Reactive Oxygen Species and Lipid Signaling in Cardiac Myocytes -- Inflammatory Signaling, Fibrosis, and Cardiac Function -- Neural Regulation of Cardiac Rhythm -- Reverse Cholesterol Transport in Atherosclerotic Cardiovascular Disease -- Progression of the Atherosclerotic Plaque Regression -- Role of Bioactive Lipid, Phosphatidic Acid in Statin-Induced Myotoxicity -- Cell-to-Cell Communication in the Vascular Endothelium -- The Bioactive Phospholipid, Lysophosphatidic Acid Regulates Vascular Endothelial Barrier Integrity -- Role of Lipid Mediators in Regulation of Vascular Endothelial Barrier Integrity and Function -- Role of Iron in Diabetic Vascular Endothelial Dysfunction -- Acknowledgments -- Contents -- Authors Biography -- Part I: Cardiac Signaling -- Calcium-Dependent Signaling in Cardiac Myocytes -- Introduction -- Physiology -- Pathophysiology -- Heart Failure -- Arrhythmias -- Ca-Dependent CaMKII Signaling in the Cardiac Myocyte -- Background -- Ca-Dependent CaMKII Signaling in Cardiac Myocyte Function and Disease -- CaMKII Structure and Ca-Dependent Activation -- Posttranslational Modifications of CaMKII as Novel Mechanisms of Cardiac Disease -- Cardiac Myocyte Remodeling and Ultrastructural Change -- Background -- Ultrastructural (T-Tubule) Remodeling -- RyR Remodeling -- Consequence of Structural Remodeling on Spatiotemporal Factors of Ca Release -- Potential Treatments -- Conclusions and Research Frontiers -- Spatial and Temporal Heterogeneity of Ca-Dependent Signaling -- Considerations for Therapy -- References -- Organization of Ca2+ Signaling Microdomains in Cardiac Myocytes -- Introduction -- Calcium Signaling in Cardiomyocytes. , Calcium Signaling Microdomains in Cardiomyocytes -- TT/jSR Microdomains in Systolic and Diastolic Calcium Handling -- Organization of cBIN1 and JP2 Microdomains at TT/jSR Membrane -- Calcium Signaling at the cBIN1 and Other TT/jSR Microdomains -- TT/jSR Microdomains, Calcium Signaling, and Heart Failure -- Ankyrin-Spectrin Microdomains in Calcium Signaling -- Organization of Ankyrin B-βII Spectrin Microdomains -- Ankyrin-Spectrin Microdomain-Regulated Calcium Signaling -- Ankyrin-Spectrin Microdomains in Cardiovascular Diseases -- Caveolae Microdomains in Calcium Signaling and Stress Response -- Organization of Caveolae Microdomains in Cardiomyocytes -- Caveolae-Related Organization of Calcium Signaling -- Caveolae, Calcium Signaling, and Disease -- Conclusions and Future Perspectives -- References -- Stress Kinase Signaling in Cardiac Myocytes -- Introduction -- Stress Kinase MAPK Signaling in the Heart -- JNK -- P38 -- ERK -- MAPKs and Calcium Homeostasis in Myocytes -- Normal and Abnormal Calcium (Ca2+) Signaling in Myocytes -- MAPKs in Stress-Evoked Ca2+ Mishandling in Myocytes -- MAPKs and Ca Handling Proteins in Myocytes -- MAPKs and Molecular Remodeling in Myocytes -- MAPKs and Gene Regulation in Myocytes -- MAPKs and Apoptotic Signaling Pathways in Stress-Exposed Myocytes -- JNK and Apoptotic Signaling Pathways in Myocytes -- p38 and Apoptotic Signaling Pathways in Myocytes -- ERK and Apoptotic Signaling Pathways in Myocytes -- Dynamic Relationships of MAPKs in Pathological Cardiac Remodeling in Stressed Hearts -- MAPKs and Therapeutic Potentials -- References -- Intracellular Cardiac Signaling Pathways Altered by Cancer Therapies -- Part I: Introduction -- Tyrosine Kinase Inhibitor Therapy -- Immune Checkpoint Therapy -- CAR T-Cell Therapy -- Part II: Tyrosine Kinases Inhibitor Therapy -- Tyrosine Kinase Signaling. , Abnormal Tyrosine Kinase Activity and Signaling in Cancer -- Tyrosine Kinase Inhibitors -- Tyrosine Kinase Receptors and Cardiomyopathy -- VEGF/VEGFR Signaling -- PDGF/ PDGFR Signaling -- c-KIT Signaling -- TKI-Induced Cardiovascular Dysfunction -- Hypertension -- Arrhythmias -- TKIs and Ion Homeostasis -- TKI-Mediated Potassium Ion Channel Dysfunction -- TKI Dysregulation of Calcium-Mediated Signaling -- TKIs and Sodium Channels: An Unexplored Territory -- TKIs and Heart Failure -- TKIs and Thromboembolism -- Monitoring and Treatment of TKI-Induced Cardiotoxicity -- Part III: Immune Checkpoint Inhibitors -- T-Cell Activation and Regulation -- Mechanisms of ICI-Mediated Cardiac Disorders -- Arrhythmias -- Myocarditis and Pericarditis -- Heart Failure -- Monitoring and Treatment of ICI-Associated Cardiotoxicity -- Part IV: CAR T-Cell Immunotherapy -- CAR T-Cell Mechanism of Action -- Proposed Mechanisms of Cardiotoxicity in CAR T-Cell Therapy -- JAK/STAT Signaling Pathway -- IL-6 -- TNFα -- Interleukin 1 -- Off-Target Affects -- Monitoring of CAR T-Cell Associated Cardiotoxicity -- Current and Proposed Treatments for CAR T-Cell-Induced Cardiotoxicity -- References -- Protein Phosphatase Signaling in Cardiac Myocytes -- Introduction -- The Kinase-Phosphatase Axis -- Protein Phosphatase Families and Genetics -- Localization and Binding Partners of Protein Phosphatases -- Mouse Models -- Protein Phosphatases in Cardiovascular Disease -- PP1 in Cardiovascular Disease -- PP2A in Cardiovascular Disease -- PP2B in Cardiovascular Disease -- Conclusions and Future Directions -- References -- Metabolic Regulation of Mitochondrial Dynamics and Cardiac Function -- Mitochondrial Dynamics: Fusion and Fission Events -- Diabetes-Related Cardiac Ischemia and Reperfusion Injury -- Diabetes-Related Cardiac Chronic Remodeling, Hypertrophy, and Failure. , Metabolic Control of Mitochondrial Dynamics: The Role of AMPK -- Concluding Remarks -- References -- NADPH Oxidase System Mediates Cholesterol Secoaldehyde-Induced Oxidative Stress and Cytotoxicity in H9c2 Cardiomyocytes -- Introduction -- Materials and Methods -- Chemicals, H9c2 Cardiomyocytes, and Cell Culture Supplies -- Synthesis of Cholesterol Secoaldehyde -- Cell Culture and Treatments -- Cell Proliferation and Metabolism -- Trypan Blue Exclusion Assay -- Measurement of Intracellular Peroxides -- Measurement of Hydrogen Peroxide -- Thiobarbituric Acid-Reactive Substances (TBARs) -- Measurement of Reduced Glutathione Levels -- Assay of Superoxide Dismutase Activity -- Measurement of Mitochondrial Transmembrane Potential -- Western Blot Analysis -- Statistical Analysis -- Results -- Apocynin Exacerbates While DPI Reduces the ChSeco-Induced Cytotoxic Response in H9c2 Cardiomyocytes -- NOS Inhibitors Attenuate the Formation of Peroxide or Peroxide-Like Substances in ChSeco-Exposed H9c2 Cardiomyocytes -- Apocynin Lowers the GSH Levels in ChSeco-Exposed Cardiomyocytes -- Apocynin But Not DPI Enhances the ChSeco-Induced Activation of SOD Activity in H9c2 Cardiomyocytes -- Apocynin and DPI Pretreatment in H9c2 Cardiomyocytes Reduces TBARs Formed in Response to the Exposure of ChSeco -- ChSeco-Induced Loss in Mitochondrial Transmembrane Potential Is Reversed by Pretreatments with Apocynin and DPI -- ChSeco-Induced Overexpression of pp38 and pSAPK in H9c2 Cardiomyocytes Is Mitigated by Pretreatments with Apo and DPI -- Discussion -- Conclusion -- References -- Lipid Mediators in Cardiovascular Physiology and Disease -- Introduction -- Lipid Mediators -- Oxylipins -- PUFA Reservoirs -- Oxylipin Synthesis -- Cyclooxygenase-Derived Oxylipins -- Lipoxygenase-Derived Oxylipins -- Cytochrome P450-Derived Oxylipins -- Conclusion and Future Perspectives. , References -- Cardiac Inflammasome and Arrhythmia -- Introduction -- Cardiac Electrophysiology -- Pathophysiology of AF -- Inflammasome Signaling -- Cardiac Inflammasome Signaling and Arrhythmogenesis -- Inflammasome-Mediated Pathogenesis of AF -- Nlrp3 Inflammasome Links AF Risk Factors to Atrial Arrhythmogenesis -- Nodal Signaling Points of Nlrp3 Activation -- Therapeutic Potential of Targeting the Cardiac NLRP3 Inflammasome -- Summary and Future Perspectives -- References -- Myocardial Fibrosis: Cell Signaling and In Vitro Modeling -- Introduction -- The Normal Myocardium -- Myocardial Fibrosis -- Modeling Myocardial Fibrosis -- Mechanotransduction -- Cell-Cell and Cell-ECM Interactions -- Pro-Fibrotic Soluble Mediators -- Conclusion -- References -- Neural Regulation of Cardiac Rhythm -- Introduction -- Neuronal Anatomy and Organization -- Cardiac Responses to Neurochemicals -- Adrenergic Signaling -- Muscarinic Signaling -- Co-transmission -- In vitro Models to Study Neural Regulation of Cardiac Rhythm -- Co-cultures -- Isolated Heart and Tissue Preparations -- Conclusions -- References -- Part II: Vascular Signaling -- Mechanisms of Lipoproteins and Reverse Cholesterol Transport in Atherosclerotic Cardiovascular Disease -- Introduction -- Lipoproteins Involved in Cholesterol Transport -- The Reverse Cholesterol Transport Pathway -- Mechanisms of Diseases Associated with Atherosclerotic CVD -- Genetic Predisposition to Cholesterol-Driven Cardiovascular Disease -- Therapeutic Approaches Targeting Lipoproteins -- LDL-C-Targeted Therapies -- HDL-C-Targeted Therapies -- References -- Atherosclerotic Plaque Regression: Future Perspective -- Introduction -- Development of Atherosclerotic Plaque and Formation of Primary Oxidation Products -- Role of Protein Carbonyls in Atherosclerotic Plaque Progression -- Factors Affecting Plaque Regression. , Increasing HDL Cholesterol.

Additional Edition: Print version: Parinandi, Narasimham L. Cardiovascular Signaling in Health and Disease Cham : Springer International Publishing AG,c2022 ISBN 9783031083082

Language: English

Keywords: Llibres electrònics

UID:

Format: 1 Online-Ressource (XVIII, 527 p. 83 illus., 59 illus. in color).

Edition: 1st ed. 2022

ISBN: 978-3-031-08309-9

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08308-2

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08310-5

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08311-2

Language: English

DOI: 10.1007/978-3-031-08309-9

URL: Volltext  (URL des Erstveröffentlichers)

UID:

Format: 1 Online-Ressource (XVIII, 527 p. 83 illus., 59 illus. in color).

Edition: 1st ed. 2022

ISBN: 978-3-031-08309-9

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08308-2

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08310-5

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-031-08311-2

Language: English

DOI: 10.1007/978-3-031-08309-9

URL: Volltext  (URL des Erstveröffentlichers)