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Prevention and Treatment of Atherosclerosis : Improving State-Of-the-Art Management and Search for Novel Targets.

Bibliographic Details
Main Author: von Eckardstein, Arnold.
Other Authors: Binder, Christoph J.
Format: eBook
Language:English
Published: Cham : Springer International Publishing AG, 2022.
Edition:1st ed.
Series:Handbook of Experimental Pharmacology Series
Subjects:
Electronic books.
Online Access:Click to View
Table of Contents:
  • Intro
  • Preface
  • Acknowledgement
  • Contents
  • Part I: Improving the Treatment of Established Targets
  • Diet, Lifestyle, Smoking
  • 1 Diet
  • 1.1 Dietary Fat (Table 1)
  • 1.1.1 Effects on CVD Risk Factors
  • 1.1.2 Effects on CVD Events
  • 1.2 Dietary Carbohydrates (Table 1)
  • 1.2.1 Effects on CVD Risk Factors
  • 1.2.2 Effects on CVD Events
  • 1.3 Salt (Table 1)
  • 1.3.1 Effects on CVD Risk Factors
  • 1.3.2 Effects on CVD Events
  • 2 Physical Activity
  • 3 Smoking
  • References
  • Blood Pressure-Lowering Therapy
  • 1 Introduction
  • 2 Non-pharmacological Therapy
  • 2.1 Salt Restriction
  • 2.2 Reduce Alcohol Intake
  • 2.3 Weight Loss and Avoidance of Overweight and Obesity
  • 2.4 Regular Physical Activity
  • 3 Pharmacological Therapy for the Treatment of Arterial Hypertension
  • 3.1 Who Should Be Treated with Pharmacological Therapy?
  • 3.2 Choice of Initial Antihypertensive Agents
  • 3.3 Combination Therapy
  • 3.4 Direct Effects of Antihypertensive Drugs on Atherosclerosis
  • 3.4.1 ARBs and ACE Inhibitors
  • 3.4.2 Diuretics
  • 3.4.3 Calcium Antagonists
  • 3.4.4 Beta-Blockers
  • 3.4.5 Mineralocorticoid Receptor Antagonists
  • 4 Perspectives of Future Antihypertensive Therapy
  • 4.1 Unresolved Medical Needs
  • 4.2 New Drug Developments
  • 4.3 Device Therapy
  • 5 Conclusion
  • References
  • Glycaemic Control in Diabetes
  • 1 Cardiovascular Risk in Diabetes
  • 2 Microvascular End-Organ Damage and Cardiovascular Risk
  • 3 Role of Hyperglycaemia for Micro- and Macro-vascular Complications
  • 4 Role of Hyperglycaemia in Reducing Vascular Risks in Type 1 Diabetes
  • 5 Efficacy Trials of Glucose Lowering in Type 2 Diabetes
  • 6 Cardiovascular Safety Studies in Type 2 Diabetes
  • 7 GLP-1 Receptor Agonists (GLP-1-RA)
  • 8 SGLT (Sodium Glucose Transporter) 2 Inhibitors
  • 9 Mechanisms of Action for Cardio-Renal Protection Through SGLT-2 Inhibition.
  • 10 Change in Guidelines and Clinical Recommendations
  • 11 Perspectives: Fat Partitioning as a New Target of Diabetes Drugs
  • References
  • LDL-Cholesterol-Lowering Therapy
  • 1 Introduction
  • 2 Statins in the Prevention of Cardiovascular Disease
  • 3 Non-statin Cholesterol-Lowering Drugs
  • 3.1 Ezetimibe
  • 3.2 PCSK9 Inhibitors
  • 3.2.1 Evolocumab
  • 3.2.2 Alirocumab
  • 3.3 Lomitapide
  • 3.4 Mipomersen
  • 4 Cholesterol-Lowering Drugs Under Clinical Development
  • 4.1 Inclisiran
  • 4.2 Bempedoic Acid
  • 5 The Future of Cholesterol Lowering
  • 5.1 ANGPTL3-LRx
  • 6 Conclusions
  • References
  • Antithrombotic Therapy: Prevention and Treatment of Atherosclerosis and Atherothrombosis
  • 1 Atherogenesis and the Role of Blood Coagulation Components
  • 1.1 Blood Coagulation: Impact on Vascular Endothelial Cells
  • 1.2 Platelets and Extracellular Vesicles
  • 1.3 Antiplatelet Agents and Atherosclerosis
  • 1.4 Coagulation Proteases
  • 2 From Atherosclerosis to Atherothrombosis
  • 3 Antithrombotic Therapy: Clinical Principles and Applications
  • 3.1 Single Antiplatelet Agents: Mode of Action and Side Effects
  • 3.2 Primary Prevention in the Population
  • Selecting the Right Subject?
  • 3.3 Primary Prevention in Subjects with Atherosclerosis
  • 3.4 Secondary Prevention of Atherothrombosis in Patients with Arterial Vascular Disease
  • 4 The Effects of Antithrombotic Therapy on the Vessel Wall and Atherogenesis: Clinical Relevance?
  • 5 Novel Antiplatelet and Anticoagulant Targets
  • References
  • Part II: Novel Drug Developments Addressing Predefined Targets
  • Metabolism of Triglyceride-Rich Lipoproteins
  • 1 Introduction
  • 2 Hepatic Formation and Secretion of VLDL
  • 3 Regulators of Hepatic VLDL Secretion
  • 4 Synthesis and Secretion of Chylomicrons from the Intestine
  • 5 Disorders of the Synthesis of TRLs
  • 6 Metabolism of Triglyceride-Rich Lipoproteins.
  • 7 Deciphering the Pathogenesis of Hypertriglyceridemia
  • 8 Regulation of Hydrolysis of TRLs and the LPL Pathway
  • 9 Role of Triglyceride-Rich Lipoproteins in Atherogenesis
  • 10 Therapies to Reduce Triglyceride-Rich Lipoproteins
  • 11 Development of Novel Interventions
  • 12 Conclusion
  • References
  • High Density Lipoproteins: Is There a Comeback as a Therapeutic Target?
  • 1 Introduction
  • 2 Possible Reasons for HDL-Cś Clinical Futility
  • 2.1 Lack of Causality
  • 2.2 Epidemiology and Human Genetics Disprove ``the Higher the Better ́́Concept
  • 2.3 Limitations of HDL Modifying Drugs
  • 2.3.1 Neither Fibrates nor Nicotinic Acid Specifically Target HDL Metabolism
  • 2.3.2 CETP Inhibitors Block Rather than Promote Reverse Cholesterol Transport
  • 2.3.3 Combination with High-Intensity Statins: The Winner Takes it All
  • 2.4 Wrong Biomarker ``the Good Cholesterol ́́
  • 3 Consequences and Perspectives
  • 3.1 The Search for Novel HDL-Biomarkers
  • 3.2 Ongoing and Novel Drug Developments
  • 3.2.1 Reconstituted HDL, apoA-I Mimetic Peptides, and Recombinant LCAT
  • 3.2.2 Apabetalone
  • 3.2.3 PPAR Modulators
  • 3.2.4 ANGPTL3 and Endothelial Lipase
  • 3.2.5 ApoC-III Inhibition
  • 3.2.6 HDL-C Lowering Therapies: Probucol and Androgens
  • 3.3 Other Disease Targets
  • 3.3.1 Diabetes
  • 3.3.2 Chronic Kidney Disease
  • 3.3.3 Infections
  • 3.3.4 Autoimmune Diseases
  • 3.3.5 Cancer
  • 3.3.6 Behind the Blood Brain Barrier: Alzheimerś Disease and Age Related Macular Degeneration
  • 3.4 Implications for Nowadayś Clinical Practice
  • References
  • Lipoprotein(a)
  • 1 Introduction
  • 2 Sites of Production and Catabolism of Lp(a)
  • 3 Physiology and Pathophysiology of Lp(a)
  • 4 Genetic Control of Lp(a) Concentrations
  • 5 Lp(a) Concentrations and Risk for CVD
  • 5.1 Searching for Lp(a) Thresholds Associated with an Increased Coronary Artery Disease Risk.
  • 5.2 Lp(a) and Other Vascular Diseases
  • 5.3 Differences Between Primary and Secondary Prevention Studies
  • 5.4 Is Lp(a) an Independent Risk Factor for CVD?
  • 6 What Evidence Do We Have for a Causal Association of High Lp(a) with CVD?
  • 7 RNA-Targeting Therapies to Specifically Lower Lp(a)
  • 7.1 Antisense Oligonucleotides (ASO) Against Apolipoprotein(a)
  • 7.2 Short Interfering RNA (siRNA) to Target Apo(a)
  • 8 Other Lipid-Lowering Drugs and Therapies with Possible Influence on Lp(a) Concentrations and Clinical Outcomes
  • 8.1 Lipoprotein Apheresis
  • 8.2 PCSK9 Inhibitors
  • 8.3 Statins
  • 8.4 Drugs That Are Probably No Longer Followed for Lp(a)-Lowering Potential
  • 9 Therapeutic Lowering of Lipoprotein(a): How Much Is Enough?
  • 10 Conclusions
  • References
  • Nonalcoholic Fatty Liver Disease
  • 1 Epidemiology
  • 1.1 Definition, Prevalence, and Incidence of NAFLD
  • 1.2 Association with Other Diseases
  • 1.3 Clinical, Economic, and Social Burden of NAFLD
  • 2 Pathophysiology of NAFLD
  • 2.1 Intrahepatic Disturbances During NAFLD
  • 2.1.1 Lipo- and Glucotoxicity
  • 2.1.2 Oxidative Stress and Mitochondrial Dysfunction
  • 2.1.3 Hepatic Inflammation and Fibrosis
  • 2.2 Metabolic Crosstalk in NAFLD
  • 2.3 Genetic Predisposition to NAFLD
  • 3 Therapeutics
  • 3.1 Dietary/Lifestyle Intervention and Bariatric Surgery
  • 3.2 Targeting Lipotoxicity
  • 3.3 Targeting Insulin/Glucose Metabolism
  • 3.4 Targeting Hepatic Inflammation and Fibrosis
  • 3.5 Targeting Bile Acid Metabolism
  • 4 Conclusion
  • References
  • Prevention and Treatment of Atherosclerosis: The Use of Nutraceuticals and Functional Foods
  • 1 Introduction
  • 2 Red Yeast Rice
  • 2.1 Untoward Effects
  • 3 Phytosterols and Phytostanols
  • 3.1 Untoward Effects
  • 4 Berberine
  • 4.1 Untoward Effects
  • 5 Fiber
  • 5.1 Untoward Effects
  • 6 Supplements in the Pipeline
  • 6.1 Astaxanthin.
  • 6.2 Hydroxytyrosol
  • 6.3 Probiotics
  • 6.4 Bergamot
  • 7 Conclusions
  • References
  • Part III: Hypothesis Based Approaches to Unravel Novel Targets
  • Novel Adipose Tissue Targets to Prevent and Treat Atherosclerosis
  • 1 Introduction
  • 2 Types of Adipose Tissue and Their Impact on Cardiovascular Disease
  • 2.1 White Adipose Tissue
  • 2.2 Thermogenic Adipose Tissue
  • 2.3 Perivascular Adipose Tissue
  • 3 Therapies Targeting Adipose Tissue with Proven Clinical Efficacy in the Treatment of Atherosclerosis
  • 3.1 Peroxisome Proliferator-Activated Receptor-γ (PPARγ) Agonists
  • 3.2 Niacin
  • 3.3 Renin-Angiotensin System Blockade
  • 4 Novel Therapeutic Targets in Adipose Tissue for Treatment of Atherosclerosis
  • 4.1 Promoting Lipoprotein Disposal and Lipid Storage in Adipose Tissues
  • 4.2 Boosting Thermogenic Activation
  • 4.3 Targeting Inflammation in Adipose Tissue
  • 4.4 Hormones Derived from Thermogenic Adipose Tissue
  • 4.5 De Novo Lipogenesis-Derived Lipokines
  • 5 Future Directions
  • References
  • Microbiome and Cardiovascular Disease
  • 1 Introduction
  • 2 Gut and Oral Microbiome Communities: Potential Drivers of ASCVD?
  • 2.1 Other Microbiome Community Members
  • 2.1.1 Viruses and Bacteriophages
  • 3 Microbiome-Derived Metabolites
  • 3.1 TMAO
  • 3.2 Imidazole-Propionate
  • 3.3 Short-Chain Fatty Acids
  • 3.4 Other Microbiome-Produced Metabolites Associated with ASCVD
  • 4 Bile Acids
  • 4.1 Bile Acid Metabolism
  • 4.2 Regulation by Bile Acids
  • 5 Summary and Future Perspectives
  • References
  • Smooth Muscle Cell-Proteoglycan-Lipoprotein Interactions as Drivers of Atherosclerosis
  • 1 Introduction
  • 2 Smooth Muscle Cell Phenotype Switch and Extracellular Matrix Production
  • 3 Extracellular Matrix (ECM)
  • 3.1 Fibrillar Matrix
  • 3.2 Proteoglycans: Non-fibrillar Components of the ECM
  • 3.2.1 Versican
  • 3.2.2 Biglycan
  • 3.2.3 Decorin.
  • 3.2.4 Perlecan.

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