Oxidative Stress : A Focus on Cardiovascular Disease Pathogensis.
Material type:
- text
- computer
- online resource
- 9781616683597
- 616.1/07
- RC669.9 -- .O97 2011eb
Intro -- OXIDATIVE STRESS -- A FOCUS ON CARDIOVASCULAR DISEASE PATHOGENESIS -- CARDIOLOGY RESEARCH AND CLINICAL DEVELOPMENTS -- OXIDATIVE STRESS A FOCUS ON CARDIOVASCULAR DISEASE PATHOGENESIS -- CONTENTS -- PREFACE -- CHAPTER 1- OXIDATIVE STRESS AND EARLY ORIGINS OF CARDIOVASCULAR DISEASE (CVD) -- CHAPTER 2- DIABETES, ITS VASCULAR COMPLICATIONS AND OXIDATIVE STRESS -- CHAPTER 3- ROLE OF OXIDATIVE STRESS IN DIABETIC KIDNEY DISEASE -- CHAPTER 4- OXIDATIVE STRESS AND FAMILY HISTORY OF CARDIOVASCULAR DISEASE -- CHAPTER 5 - GENETIC REMODELING AND CARDIOVASCULAR DISEASE -- CHAPTER 6 - OXIDATIVE STRESS AND THE MECHANISMS OF ATHEROSCLEROSIS -- CHAPTER 7 - NUTRIGENOMICS, OXIDATIVE STRESS AND MECHANISMS OF CARDIOVASCULAR DISEASE -- CHAPTER 8 - ALCOHOL, OXIDATIVE STRESS AND MECHANISMS OF CARDIOVASCULAR DISEASE -- CHAPTER 9 - VITAMINS AND CARDIOVASCULAR DISEASE -- CHAPTER 10 - DIABETES MELLITUS AND OXIDATIVE STRESS -- CHAPTER 11- OXIDIZED LDL AND CARDIOVASCULAR DISEASE -- CHAPTER 12 - EFFECT OF CIGARETTE SMOKE ON OXIDATIVE STRESS AND VASCULAR ENDOTHELIAL FUNCTION -- CHAPTER 13 - MECHANISMS OF ENDOTHELIAL PROGENITOR CELLS SENESCENCE IN CARDIOVASCULAR DISEASE -- CHAPTER 14 - STEM CELLS, OXIDATIVE STRESS AND NEW TREATMENT STRATEGIES FOR CARDIOVASCULAR DISEASES -- CHAPTER 15 - NA+/H+ EXCHANGER 1 (NHE-1) REDOX-REGULATED GENE AND INTRACELLULAR TARGET FOR THE REDOX CONTROL OF CELL DEATH SENSITIVITY -- OXIDATIVE STRESS AND EARLY ORIGINS OF CARDIOVASCULAR DISEASE -- ABSTRACT -- INTRODUCTION -- THE PATHOLOGICAL EVENTS IN EARLY CVD -- Endothelial Dysfunction -- Lipid Infiltration within Arterial Walls -- Macrophage Accumulation -- Circulating Blood-Induced Endothelial Stress -- Lipoprotein Oxidation -- Thrifty Phenotype' Hypothesis and Fetal Programming of CVD -- OXIDATIVE STRESS AND PROGRAMMING OF FETAL CVD.
INFLAMMATORY RESPONSE AND EXPRESSION OF NF-ΚB- DEPENDENT GENES IN THE PROGRAMMING OF FETAL CVD -- EPIGENETIC REGULATION OF GENE EXPRESSION IN CVD PROGRAMMING -- MATERNAL HYPERCHOLESTEROLEMIA ENHANCES POSTNATAL CVD -- Maternal Hypercholesterolemia Enhances Atherosclerosis -- Maternal Hypercholesterolemia and Developing Fetal Heart -- Pathophysiological Implications -- DIET AND THE MATERNO/FETAL CHOLESTEROL HYPOTHESIS -- THERAPEUTIC IMPLICATIONS -- ACKNOWLEDGEMENTS -- REFERENCES -- DIABETES, ITS VASCULAR COMPLICATIONS AND OXIDATIVE STRESS -- ABSTRACT -- INTRODUCTION -- DIABETES AND ITS COMPLICATIONS -- Prevalence and Common Types of Diabetes -- Diabetes Complications and Risk Factors -- OXIDATIVE STRESS IN DIABETES -- Definition and Central Roles -- MEASURES OF OXIDATIVE STRESS -- 1. Lipid Peroxidation -- 2. Glutathione Levels -- 3. Glutathione Peroxidase and Reductase -- 4. Catalase -- 5. Superoxide Dismutase (SOD) -- 6. Vitamins -- 7. Nitric Oxide Related -- 8. Advanced Glycation End-Products -- GLYCATION AND OXIDATIVE STRESS MEASUREMENT IN CLINICAL RESEARCH -- ARE SHORTER TERM MEASURES OF OXIDATIVE AND AGE STRESS OF VALUE? -- Isoprostanes -- EXPLORING OXIDATIVE STRESS MECHANISMS IN DIABETES -- Basic Science Research Tools -- Measurement of ROS In Vivo or Ex Vivo -- Animal Models of Oxidative Stress in Diabetes -- CLINICAL STUDIES OF ANTI-OXIDANTS IN PATIENTS WITH DIABETES -- CONCLUSION -- GRANT SUPPORT -- REFERENCES -- ROLE OF OXIDATIVE STRESS IN DIABETIC KIDNEY DISEASE -- SUMMARY -- METHODOLOGY -- INTRODUCTION -- Diabetic Kidney Disease: Epidemiology -- Diabetic Kidney Disease: Pathogenesis -- Mortality of DKD -- Therapeutic Strategies of DKD -- ROS GENERATION IN DKD -- Physiological Role of ROS -- Physiological Mitochondrial Oxidation Phosphorylation -- Role of ROS in DKD -- Increased Mitochondrial ROS Generation in DKD.
1. Glucose Autooxidation and Glycolysis -- 2. Primary Inherited Mitochondrial Dysfunction -- 3. Mitochondrial Uncoupling of the Respiratory Chain -- 4. Advanced Glycation End Products (AGE) -- 5. Sorbitol/Polyol Flux Pathway -- 6. Cytokines and Growth Factors-Signal Transduction and Amplification -- 7. NAD(P)H Oxidase Pathway -- 8. Defective Glutathione Pathway -- 9. Xanthine Oxidase Pathway -- 10. Uncoupling of Nitric Oxide Synthetase (NOS) -- 11. Altered Activity of Antioxidant Enzymes -- 12. Role of Catalytic Iron in DKD -- 13. Sequestration of Nitric Oxide (NO) to Peri-oxynitrite (ONOO-) -- ROS INHIBITION FOR THE TREATMENT OF DKD -- 1) Inhibition or Blockade of Renin-Angiotensin System (RAS) -- 2. Inhibition of Protein Kinase C -- 3. Inhibitors of Transforming Growth Factor-β -- 4. Inhibition of Nonenzymatic Glycation -- 5. Removal of Catalytic Iron -- 6. Role of Pentoxifylline -- 7. Selective Mitochondrial Antioxidants -- 8. Statins for DKD -- 9. Vitamin C and E -- 10. Sodium Bicarbonate for the treatment of DKD -- 11. N-acetylcysteine (NAC) for the Treatment of DKD -- 12. Induction of Transcription Factor Nrf2: Bardoxolone Methyl -- 13. Other Potential Antioxidants for the Treatment of DKD -- CONCLUSION -- ACKNOWLEDGMENTS -- DISCLOSURE OF AUTHORS -- GLOSSARY TERMS -- REFERENCES -- OXIDATIVE STRESS AND FAMILY HISTORY OF CARDIOVASCULAR DISEASE -- ABSTRACT -- ABBREVIATIONS -- INTRODUCTION -- FAMILY HISTORY AND CVD RISK PREDICTION -- FAMILY HISTORY TOOLS -- THE MANY FACTORS INVOLVED IN THE FAMILIAL AGGREGATION OF CVD -- OXIDATIVE STRESS IN CVD -- CONCLUSION -- REFERENCES -- GENETIC REMODELING AND CARDIOVASCULAR DISEASE -- ABSTRACT -- INTRODUCTION -- IMPACT OF GENE VARIANTS ON CARDIOVASCULAR PHENOTYPE -- GENE - ENVIRONMENT INTERACTIONS -- PHARMACOGENETICS -- CURRENT METHODOLOGICAL APPROACHES -- CONCLUSION -- ACKNOWLEDGEMENTS -- REFERENCES.
OXIDATIVE STRESS AND THE MECHANISMS OF ATHEROSCLEROSIS -- ABSTRACT -- INTRODUCTION -- SOURCE OF ROS IN ATHEROSCLEROSIS -- NADPH Oxidase -- Myeloperoxidase -- Xanthine Oxidase -- Mitochondrial Electron Transport Chain -- Nitric Oxide Synthases -- OXIDATIVE STRESS AND THE ATHEROSCLEROTIC DISEASE -- Markers of Oxidative Stress -- Cardiovascular Risk Factors -- Cardiovascular Events -- ROLE OF ANTIOXIDANTS -- CONCLUSION -- REFERENCES -- NUTRIGENOMICS, OXIDATIVE STRESS AND MECHANISMS OF CARDIOVASCULAR DISEASE -- ABSTRACT -- INTRODUCTION -- ENDOTHELIAL DYSFUNCTION AND ATHEROSCLEROSIS -- RISK FACTORS FOR CARDIOVASCULAR DISEASE -- WHAT IS "NUTRIGENOMICS" AND WHY IS IT SO IMPORTANT? -- ANTIOXIDANT COMPOUNDS, NUTRIGENOMICS AND CARDIOVASCULAR DISEASE -- Isoflavones -- Resveratrol -- Alpha-tocopherol -- FATTY ACIDS, NUTRIGENOMICS AND CARDIOVASCULAR DISEASE -- CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES -- ALCOHOL, OXIDATIVE STRESS AND MECHANISMS OF CARDIOVASCULAR DISEASE -- ABSTRACT -- INTRODUCTION -- HISTORICAL PERSPECTIVE -- EPIDEMIOLOGIC STUDIES -- POLYPHENOLS/FLAVENOIDS -- LIPID METABOLISM -- REACTIVE OXYGEN SPECIES -- GENE EXPRESSION -- VASCULAR SMOOTH MUSCLE CELLS, PLATELETS AND COAGULATION -- INFLAMMATORY PROCESSES -- TOXIC EFFECTS OF ALCOHOL -- CONCLUSION -- REFERENCES -- VITAMINS AND CARDIOVASCULAR DISEASE -- ABSTRACT -- INTRODUCTION -- STUDY RESULTS -- 1. Animal Studies -- 2. Observational Studies -- Vitamin E- -- Vitamin C and Beta Carotene (Carotenoids) -- 3. Randomised Controlled Trials (RCTs) -- Vitamin E -- Vitamin C, Beta-Carotene (Carotenoids) -- ROLE OF SUPPLEMENTATION -- 1. Vitamin Type, Single or Combination Supplementation -- Vitamin Type -- Single or Combination Supplementation -- Dose of Vitamin- Mega-Doses or Suboptimal Doses -- Role of Subgroup Targeting -- Gender and Age -- Smokers -- Cardiovascular Risk Factors.
When to Supplement -- CONCLUSION -- REFERENCES -- DIABETES MELLITUS AND OXIDATIVE STRESS -- ABSTRACT -- INTRODUCTION -- ROLE OF OXIDATIVE STRESS IN DIABETES -- A. Uncoupling of Oxidative Phosphorylation -- B. Endothelial Nitric Oxide Synthase Uncoupling -- 1. Glutathione Depletion (Increased Polyol Pathway Flux) -- 2. Activation of Protein Kinase C (PKC) -- 3. Increased Advanced Glycation End-Product Formation -- 4. Increased Hexosamine Pathway Flux -- DIABETES AND CARDIOVASCULAR DISEASE -- A. Diabetes and Ischemic Heart Disease -- 1. Endothelial Dysfunction and Plaque Initiation -- 2. Accelerated Atherogenesis and Plaque Growth -- 3. Plaque Rupture and Platelet Signaling Abnormalities -- 4. Reperfusion Injury -- B. Diabetes and Non-Ischemic Cardiomyopathy -- 1. Increased Apoptosis -- 2. Activation of the Renin-Angiotensin System -- 3. Myocardial Lipid Deposition -- 4. Small Vessel Disease -- ANTI-OXIDANT THERAPIES -- CONCLUSION -- REFERENCES -- OXIDIZED LDL AND CARDIOVASCULAR RISK -- ABSTRACT -- INTRODUCTION -- LDL SUBPOPULATIONS -- OXIDATIVE MODIFICATIONS OF LDL -- ORIGIN OF OXLDL -- CLEARANCE OF OXLDL -- PROATHEROGENIC PROPERTIES OF OXLDL -- PRO-INFLAMMATORY EFFECTS OF OXLDL -- QUANTIFICATION OF OXLDL -- BIOLOGICAL VARIABILITY -- OXLDL AS CAD RISK MARKER -- OXLDL IN THE METABOLIC SYNDROME -- OXLDL AND CARDIAC (DYS)FUNCTION -- OXLDL AND CEREBROVASCULAR DISEASE -- PREDICTION OF ACUTE CORONARY EVENTS -- OXLDL AND (PRECLINICAL) ATHEROSLEROSIS -- CONCLUSION -- REFERENCES -- EFFECT OF CIGARETTE SMOKE ON OXIDATIVE STRESS AND VASCULAR ENDOTHELIAL FUNCTION -- ABSTRACT -- INTRODUCTION -- 1. SMOKE CONSTITUENTS INVOLVED IN OXIDATIVE STRESS AND ENDOTHELIAL DYSFUNCTION -- 1.1. Free Radicals -- 1.2. Unsaturated Aldehydes -- 1.3. Metals -- 1.4. Nicotine -- 1.5. Other Chemical Substances -- 1.6. Particles -- 2. ENDOTHELIAL MOLECULAR CONSEQUENCES.
2.1. Antioxidative Defense Mechanism.
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