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Umfang: 1 online resource (500 pages).

ISBN: 9780128222591 , 012822259X

Serie: Translational epigenetics series ; Volume 24

Anmerkung: Intro -- Epigenetics in Cardiovascular Disease -- Copyright -- Contents -- Contributors -- Preface -- The burden of cardiovascular disease -- Central dogma of molecular biology -- Epigenetic mechanisms -- Epigenetic mechanisms as biomarkers and treatment targets in CVD -- The EU-CardioRNA COST Action: networking to advance science -- Presentation of the book and chapters -- Acknowledgments -- References -- Section I: Introductory information -- Chapter 1: The ever-growing burden of cardiovascular disease -- 1.1. Introduction -- 1.2. Financial load of cardiovascular disease -- 1.3. Risk factors and health(y) behaviors -- 1.3.1. Risk factors -- 1.3.1.1. Hypertension -- 1.3.1.2. Cholesterol -- 1.3.1.3. Diabetes mellitus -- 1.3.1.4. Obesity -- 1.3.2. Health behaviors -- 1.3.2.1. Smoking -- 1.3.2.2. Alcohol -- 1.3.2.3. Physical inactivity -- 1.3.2.4. Vegetable and fruit consumption -- 1.4. Cardiovascular morbidity -- 1.4.1. Incidence and prevalence of cardiovascular disease -- 1.4.1.1. Incidence and Prevalence of ischemic heart disease -- 1.4.1.2. Incidence and prevalence of stroke -- 1.4.1.3. Incidence and prevalence of peripheral vascular disease -- 1.4.1.4. Incidence and prevalence of heart failure: growing problem -- 1.4.1.5. Incidence and prevalence of atrial fibrillation -- 1.5. Disability-adjusted life years due to cardiovascular disease -- 1.6. Mortality in cardiovascular disease -- 1.7. Premature cardiovascular mortality -- References -- Chapter 2: Epigenetics concepts: An overview -- 2.1. From general concepts to molecular mechanisms -- 2.2. DNA methylation -- 2.3. Posttranslational modifications of histones -- 2.3.1. Histone acetylation -- 2.3.2. Histone methylation -- 2.3.3. Histone phosphorylation -- 2.4. Chromatin remodeling and transcription -- 2.5. Noncoding RNAs -- 2.6. RNA modifications -- 2.7. Cardiovascular epigenetics. , 2.7.1. Epigenetics and cardiac development -- 2.7.2. Postnatal growth and maturation of the heart -- 2.7.3. Adult heart disease -- 2.8. Conclusions -- Acknowledgments-Sources of funding -- References -- Chapter 3: From classical signaling pathways to the nucleus -- 3.1. Introduction -- 3.2. Ca2+-dependent changes in gene expression -- 3.2.1. Ca2+-/calmodulin-dependent kinase II -- 3.2.2. Protein kinase C -- 3.2.3. CAMTA2 -- 3.2.4. Ca2+-dependent regulation of alternative splicing -- 3.3. cAMP-dependent epigenetic regulation -- 3.3.1. Protein kinase A (PKA) -- 3.3.2. PKA and lipid droplet-associated signaling -- 3.3.3. Nuclear retention of class IIa HDACs -- 3.3.4. A-kinase-anchoring proteins (AKAPs) and cAMP compartmentalization signaling -- 3.4. Antagonistic roles of Ca2+ and cAMP signaling -- 3.5. Translational perspective -- 3.6. Future directions -- Source of funding -- References -- Section II: Epigenetics mechanisms in cardiovascular disease -- Chapter 4: DNA methylation in heart failure -- 4.1. DNA methylation in the heart -- 4.1.1. Preface -- 4.1.2. Mechanisms of DNA methylation and demethylation -- 4.1.3. Mechanisms that regulate DNA methylation and demethylation -- 4.1.4. The DNA methylation landscape -- 4.1.5. DNA methylation in the healthy heart -- 4.1.6. DNA methylation in cardiac disease -- 4.1.6.1. Studies in humans hearts -- 4.1.6.2. DNA methylation in animal models of heart failure -- 4.1.7. Targeting DNA methylation for therapy -- 4.1.8. DNA methylation signature as biomarkers for heart failure -- 4.1.9. Future outlook -- References -- Chapter 5: Histone modifications in cardiovascular disease initiation and progression -- 5.1. Introduction -- 5.1.1. DNA and chromatin structure -- 5.1.2. Histone variants -- 5.1.2.1. Histone variants in the heart -- 5.1.2.2. Histone turnover in the heart. , 5.2. Histone modifications: The fundamentals -- 5.2.1. Histone modifiers and readers -- 5.2.2. Histone acetyltransferases -- 5.2.3. Histone deacetylases (HDACs) -- 5.2.3.1. Class I HDACs -- 5.2.3.2. Class IIa and Class IIb HDACs -- 5.2.3.3. Class III HDACs: Sirtuins -- 5.2.3.4. Class IV HDAC: HDAC11 -- 5.2.3.5. Histone-independent roles of HDACs -- 5.2.4. Histone methyltransferases (HMTs) -- 5.2.4.1. Euchromatic lysine methyltransferases 1 and 2 (EHMT1/2) -- 5.2.4.2. Suppressor of Variegation 3-9 Homolog (SUV39H1/2) -- 5.2.4.3. SET and MYND domain-containing proteins (SMYDs) -- 5.2.4.4. Disruptor of telomeric silencing 1-like (DOT1L) -- 5.2.4.5. Histone arginine methyltransferases (PRMTs) -- 5.2.5. Histone lysine demethylases (KDMs) -- 5.3. Histone modifications in cardiomyocyte differentiation, development, and proliferation -- 5.3.1. Cardiomyocyte remodeling in development and disease -- 5.4. Pharmaceutical targeting of epigenetic modifiers and modifications in CVD -- 5.4.1. HDAC inhibitors (HDACi) -- 5.4.2. Histone-independent roles of HDACi -- 5.4.3. DNA methyltransferase inhibitors (DNMTi) -- 5.4.4. Bromodomain and extraterminal domain inhibition (BETi) -- 5.5. Histone profiling and personalized medicine -- 5.6. Conclusion and future perspectives -- References -- Chapter 6: RNA modifications in cardiovascular disease-An experimental and computational perspective -- 6.1. Introduction -- 6.2. m6A mRNA methylation -- 6.2.1. m6A methylases and m6A demethylases -- 6.2.2. m6A readers -- 6.3. m6A in cardiovascular disease -- 6.3.1. m6A in heart failure -- 6.3.2. m6A and regulation of cell growth -- 6.3.3. m6A and response to ischemia -- 6.4. Mechanisms and outlook -- 6.5. Modification mapping approaches -- 6.5.1. Antibody-based methods -- 6.5.1.1. MeRIP-seq/LAIC-seq -- 6.5.1.2. miCLIP -- 6.5.2. Antibody-free methods. , 6.5.2.1. Reverse transcription signatures -- 6.5.2.2. Enzymatic methylation-sensitive RNA digest -- 6.5.2.3. Nanopore direct RNA sequencing -- Acknowledgments -- References -- Chapter 7: Regulatory RNAs in cardiovascular disease -- 7.1. Introduction -- 7.2. Noncoding RNAs -- 7.2.1. MicroRNAs -- 7.2.2. Long noncoding RNAs -- 7.2.3. Circular RNAs -- 7.3. Regulatory RNAs in myocardial infarction -- 7.3.1. MiRNAs and myocardial infarction -- 7.3.2. LncRNA in myocardial infarction -- 7.3.3. CircRNAs in myocardial infarction -- 7.4. Noncoding RNAs in cardiac remodeling and heart failure -- 7.4.1. MiRNAs in cardiac remodeling and heart failure -- 7.4.2. LncRNAs in cardiac remodeling and heart failure -- 7.4.3. CircRNAs in cardiac remodeling and heart failure -- 7.5. Regulatory RNAs in arrhythmias -- 7.5.1. miRNAs in arrhythmias -- 7.5.2. LncRNAs in arrhythmias -- 7.6. Translational perspective and conclusions -- Funding -- References -- Chapter 8: Regulation of splicing in cardiovascular disease -- 8.1. RNA splicing, constitutive splicing, and alternative splicing -- 8.1.1. Splicing and noncoding RNAs -- 8.2. Regulation of RNA splicing -- 8.2.1. Gene architecture -- 8.2.2. RNA transcription and elongation speed -- 8.2.3. Variation within splice site consensus sequences -- 8.2.4. Cis-regulatory sequences and transacting factors -- 8.2.5. The epitranscriptome -- 8.2.6. Chromatin epigenetic marks -- 8.2.7. RNA secondary structures -- 8.2.8. Interactions with other RNA molecules -- 8.3. Splicing factors in the heart -- 8.4. Regulation of RNA splicing in heart disease -- 8.4.1. Myotonic dystrophy -- 8.4.2. Hypertrophic cardiomyopathy -- 8.4.3. Dilated cardiomyopathy -- 8.4.4. Arrhythmias -- 8.4.5. Heart failure -- 8.4.6. Atherosclerosis -- 8.4.7. Congenital heart defects -- 8.5. Alternative splicing: Therapeutic potential. , 8.6. Conclusions and future perspectives -- Acknowledgments -- References -- Chapter 9: Cardiac transcriptomic remodeling in metabolic syndrome -- 9.1. Oxidative stress in metabolic syndrome -- 9.2. Cardiovascular diseases and cardiac remodeling associated with the metabolic syndrome -- 9.2.1. Energy metabolism of the developing and diseased hearts -- 9.2.2. Remodeling of gene expression -- 9.2.2.1. How gene expression is controlled -- 9.2.2.2. Signal transduction in the failing heart -- Regulation of gene expression and signaling pathway activity -- Metabolic and stress-signaling pathways in the heart -- 9.2.2.3. Noncoding RNAs as controls of gene expression in HF -- miRNAs in cardiac remodeling -- Long noncoding RNAs in cardiac remodeling -- 9.2.2.4. The role of coronary microvascular inflammation in HFpEF -- 9.3. To metabolic syndrome -- 9.4. Conclusion -- References -- Chapter 10: Sex differences in epigenetics mechanisms of cardiovascular disease -- 10.1. Influence of sex in the development of cardiovascular diseases -- 10.2. Epigenetics and sex chromosomes at cardiovascular level -- 10.3. Epigenetics and sexual hormones at cardiovascular level -- 10.3.1. Mechanism of estrogen signaling -- 10.3.2. Mechanism of androgen signaling -- 10.3.3. Epigenetics and estrogen receptors -- 10.3.3.1. DNA methylation -- 10.3.3.2. Histone modification -- 10.3.3.3. Noncoding RNA -- 10.3.4. Epigenetics and androgen receptors -- 10.3.4.1. DNA methylation -- 10.3.4.2. Histone modification -- 10.3.4.3. Noncoding RNA -- 10.4. Conclusions and future directions -- Acknowledgments -- References -- Chapter 11: Epigenetics in cardiac development and human induced pluripotent stem cells -- 11.1. General introduction -- 11.2. Embryonic development of the heart -- 11.2.1. General principle -- 11.2.2. Epigenetic regulation in mammalian heart development. , 11.2.3. Models of cardiogenesis.

Weitere Ausg.: ISBN 9780128222584

Weitere Ausg.: ISBN 0128222581

Sprache: Englisch