My Account Log in

1 option

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.
Contributor:
Suri, M. B. A.
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

The Penn Libraries is committed to describing library materials using current, accurate, and responsible language. If you discover outdated or inaccurate language, please fill out this feedback form to report it and suggest alternative language.

Find

Home Release notes

My Account

Shelf Request an item Bookmarks Fines and fees Settings

Guides

Using the Find catalog Using Articles+ Using your account