Cardiovascular signaling in health and disease
| Other Authors: | , |
|---|---|
| Format: | eBook |
| Language: | Inglés |
| Published: |
Cham, Switzerland :
Springer International Publishing
[2022]
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| Subjects: | |
| See on Biblioteca Universitat Ramon Llull: | https://discovery.url.edu/permalink/34CSUC_URL/1im36ta/alma991009839130106719 |
Table of Contents:
- 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.
