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Reactive Oxygen Species in Cardiometabolic Syndrome, Neuronal Diseases and Cancer : From Bench to Its Potential Therapeutics.
Elsevier ScienceDirect eBook - Biochemistry, Genetics and Molecular Biology 2025 Available online
View online- Format:
- Book
- Author/Creator:
- Isenovic, Esma.
- Language:
- English
- Physical Description:
- 1 online resource (453 pages)
- Edition:
- 1st ed.
- Place of Publication:
- Chantilly : Elsevier, 2025.
- Summary:
- Reactive Oxygen Species in Cardiometabolic Syndrome, Neuronal Diseases and Cancer: From Bench to its Potential Therapeutics systematically summarizes findings concerning the biochemical properties of various reactive oxygen species (ROS).
- Contents:
- Front Cover
- Halftitle
- Titlepage
- Copyright
- Contents
- Contributors
- Preface
- Section I Introduction to ROS
- Chapter 1 Reactive oxygen species in general
- 1.1 Introduction
- 1.2 The basics of oxidative stress
- 1.3 Cellular sources of free radicals
- 1.4 Mitochondrial ROS production
- 1.5 Exogenous sources of ROS
- 1.6 Mechanisms of ROS-induced oxidative damage
- 1.7 Antioxidant defense
- 1.7.1 Enzymatic antioxidants
- 1.7.2 Nonenzymatic antioxidants
- 1.8 Natural antioxidant compounds in preventing os stress in various diseases
- 1.9 Conclusion and future perspectives
- Funding
- References
- Chapter 2 Reactive oxygen species signaling
- 2.1 Introduction to ROS signaling
- 2.2 Mechanisms of ROS signaling
- 2.3 ROS-activated signaling pathways
- 2.3.1 MAPK pathway
- 2.3.2 PI3K/Akt pathway
- 2.3.3 NFκB pathway
- 2.3.4 Other ROS-regulated signaling pathways
- 2.4 Ion channels targeted by ROS
- 2.5 ROS and disease pathology
- 2.5.1 Cancer
- 2.5.2 Cardiovascular diseases
- 2.5.3 Neurodegenerative diseases
- 2.6 Therapeutic targeting of ROS signaling
- 2.7 Modulation of redox-sensitive pathways
- 2.8 Conclusion and future perspectives
- Acknowledgment
- Chapter 3 ROS and regulation of gene expression
- 3.1 Introduction to ROS and regulation of gene expression
- 3.2 ROS
- 3.2.1 Defining ROS and cellular sources
- 3.2.2 Redox signaling - mechanisms of action in gene regulation
- 3.2.3 Disturbed redox homeostasis
- 3.3 ROS: Signaling molecules and regulators of gene expression
- 3.3.1 ROS and redox-sensitive transcription factors
- 3.4 ROS and regulation of gene expression in human diseases
- 3.4.1 ROS and regulation of gene expression in cancer
- 3.4.2 ROS and regulation of gene expression in cardiovascular diseases.
- 3.4.3 ROS and regulation of gene expression in neurodegenerative diseases
- 3.4.4 ROS and regulation of gene expression in metabolic disorders
- 3.5 Conclusions and future perspectives
- Abbreviations
- Section II ROS in cardiometabolic syndrome
- Chapter 4 Molecular mechanisms of reactive oxygen species effects in cardiometabolic syndrome
- 4.1 Introduction
- 4.2 Clinical criteria for CMS and its prevalence
- 4.3 Key epigenetic mechanisms in CMS
- 4.3.1 Altered DNA methylation patterns
- 4.3.2 Histone modifications in CMS
- 4.3.3 Role of microRNAs and long non-coding RNAs in CMS
- 4.4 Genetic profile in CMS
- 4.4.1 Single nucleotide polymorphisms in CMS
- 4.4.2 Copy number variations in CMS
- 4.5 Transcription factors in CMS
- 4.6 Key signal transduction pathways altered in CMS
- 4.7 Adipokines, growth factors, and other hormone signaling in CMS
- 4.8 Oxidative stress in CMS
- 4.8.1 Effect of elevated ROS on metabolic function
- 4.8.2 Oxidative modification of biomolecules
- 4.9 Hyperlipidemia and oxidative stress in CMS
- 4.9.1 LDL Metabolism and oxidative stress in CMS
- 4.10 Conclusion
- Chapter 5 Molecular mechanisms of reactive oxygen species and regulation of gene expression in cardiometabolic syndrome
- 5.1 Introduction
- 5.2 Molecular mechanisms of ROS and regulation of gene expression related to the development of IR
- 5.3 Molecular mechanisms of ros and regulation of gene expression related to pancreatic beta cell dysfunction
- 5.4 Molecular mechanisms of ROS and regulation of gene expression related to the development of hypertension
- 5.5 Molecular mechanisms of ROS and regulation of gene expression in endothelial dysfunction and dyslipidemia
- 5.6 Molecular mechanisms of ROS and regulation of gene expression related to the development of obesity
- 5.7 Conclusions.
- 5.8 Future perspectives
- Chapter 6 Antioxidant supplementation and cardiometabolic syndrome
- 6.1 Introduction
- 6.2 Antioxidant strategies
- 6.3 Antioxidant supplementation
- 6.3.1 Antioxidant supplementation in obesity
- 6.3.2 Antioxidant supplementation in polycystic ovary syndrome
- 6.3.3 Antioxidant supplementation in metabolic dysfunction-associated steatotic liver disease
- 6.3.4 Antioxidant supplementation in arterial hypertension
- 6.3.5 Antioxidant supplementation in T2DM
- 6.3.6 Antioxidant supplementation in cardiovascular disease
- 6.3.7 Antioxidant supplementation in chronic kidney disease
- 6.4 Lifestyle interventions
- 6.5 Conclusion and future perspectives
- Section III ROS and neuronal diseases
- Chapter 7 Molecular mechanisms of reactive oxygen species in neurodegenerative diseases (Alzheimer, Parkinson, etc.)
- 7.1 Introduction
- 7.1.1 Alzheimer's disease
- 7.1.2 Parkinson's disease
- 7.1.3 Amyotrophic lateral sclerosis
- 7.1.4 Huntington's disease
- 7.2 Conclusion and future directions
- Chapter 8 Reactive oxygen species and psychiatric disorders
- 8.1 Introduction
- 8.2 ROS in depression and anxiety
- 8.3 ROS and bipolar disorder
- 8.4 ROS and post-traumatic stress disorder
- 8.5 ROS and schizophrenia
- 8.5.1 The role of inflammation and ROS in schizophrenia
- 8.5.2 Dopaminergic signaling and ros formation
- 8.6 ROS and autism spectrum disorder
- 8.6.1 The role of inflammation and ros in autism spectrum disorder
- 8.6.2 Inhibition of superoxide dismutase activity
- 8.6.3 The mTORC1 pathway and ROS in autism spectrum disorder
- 8.7 Conclusions
- 8.7.1 Future perspectives
- Chapter 9 The role of antioxidant supplementation in neuronal disorders
- 9.1 Introduction
- 9.2 Oxidative stress, as canonically known, initiates neuronal damage.
- 9.3 Oxidative stress suggested autophagy pathway activation (in the Brain)
- 9.4 Oxidative stress suggested mitophagy pathway activation
- 9.5 Oxidative stress suggested ferritinophagy pathway activation
- 9.6 Oxidative stress suggested macrophage polarization activation
- 9.7 Oxidative stress could result in different types of neuronal cell death
- 9.8 Oxidative stress and brain-heart cross-talk
- 9.9 Antioxidant mechanisms and neuronal diseases
- 9.10 Recommendations and future prospective
- Section IV ROS and cancer
- Chapter 10 Reactive oxygen species (ROS) and early stage of cancer (Cancer development)
- 10.1 Introduction
- 10.2 Redox homeostasis and regulation
- 10.3 Major sources of ROS and mechanisms of ROS generation in precancerous cells
- 10.3.1 The mitochondrial electron transport chain
- 10.3.2 Peroxisomal metabolism
- 10.3.3 Endoplasmic reticulum
- 10.3.4 NADPH oxidases
- 10.3.5 Xanthine oxidase
- 10.3.6 Cyclooxygenase
- 10.3.7 Lipoxygenases
- 10.3.8 Extracellular and environmental sources
- 10.4 ROS in early tumorigenesis
- 10.5 ROS in oncogenic transformation
- 10.6 ROS and epigenetic alterations in cancer initiation
- 10.7 ROS in cell proliferation and apoptosis resistance
- 10.8 Conclusions and future remarks
- Chapter 11 Reactive oxygen species (ROS) and late-stage cancer (Cancer metastasis)
- 11.1 Introduction
- 11.1.1 The mechanisms by which ROS affects cancer metastasis
- 11.1.2 The role of ROS in cell migration
- 11.1.3 The role of ROS in cancer invasion
- 11.1.4 The role of ROS in EMT
- 11.1.5 The role of ROS in angiogenesis
- 11.1.6 The role of tumor-suppressor genes in ROS-mediated cancer metastasis
- 11.1.7 The role of microRNAs in ROS-mediated cancer metastasis
- 11.2 The role of ROS in liver cancer progression and metastasis.
- 11.2.1 The main risk factors in developing HCC
- 11.2.2 ROS in HCC genetic changes
- 11.2.3 ROS in HCC
- modifications of signaling pathways
- 11.2.4 ROS and transcription factors in HCC
- 11.2.5 ROS and autophagy
- 11.2.6 Cholangiocarcinoma
- 11.2.7 ROS and inflammation in CCA
- 11.2.8 Angiosarcoma and hepatoblastoma
- 11.3 The role of ROS in CRC progression and metastasis
- 11.3.1 ROS-mediated ECM remodeling and migration in CRC
- 11.3.2 ROS-mediated EMT in CRC
- 11.3.3 ROS-mediated angiogenesis in CRC
- 11.3.4 The role of tumor-suppressor genes in ROS-mediated progression of CRC
- 11.3.5 ROS-mediated regulation of MicroRNAs in CRC
- 11.4 The role of ROS in BC progression and metastasis
- 11.5 Conclusion and future directions
- Acknowledgments
- Conflict of interest
- Chapter 12 Antioxidant supplementation and cancer
- 12.1 Introduction
- 12.2 Role of enzymatic and non-enzymatic endogenous antioxidants in cancer
- 12.3 Role of non-enzymatic endogenous antioxidants in cancer
- 12.4 Dietary antioxidants in cancer
- 12.5 Conclusions
- 12.6 Future perspectives
- Chapter 13 Summary with concluding remarks, and future perspective
- 13.1 Summary
- 13.2 Concluding remarks
- 13.3 Future perspectives
- Index
- Back Cover.
- Notes:
- Description based on publisher supplied metadata and other sources.
- ISBN:
- 0-443-27334-0
- OCLC:
- 1532833808
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