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Author: John F. Keaney Jr. Publisher: Springer Science & Business Media ISBN: 9780792386780 Category : Medical Languages : en Pages : 404
Book Description
One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.
Author: John F. Keaney Jr. Publisher: Springer Science & Business Media ISBN: 9780792386780 Category : Medical Languages : en Pages : 404
Book Description
One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.
Author: John F. Keaney Jr. Publisher: Springer Science & Business Media ISBN: 1461546494 Category : Medical Languages : en Pages : 404
Book Description
One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.
Author: Cristina M. Sena Publisher: Frontiers Media SA ISBN: 2889630587 Category : Languages : en Pages : 158
Book Description
Oxidative stress is an underlying factor in health and disease. Reactive oxygen species are produced as a result of normal cellular metabolism. The subsequent altered redox state between the formation and the neutralization of pro-oxidants results in their increased levels and therefore leads to cellular damage. Different research disciplines have increased our knowledge of the importance of this cell redox status and the recognition of oxidative stress as a process with implications for many pathophysiological states. Genetic and environmental factors, nutrition and lifestyle may indicate a pro-oxidative and pro-inflammatory state, linked to alterations in cellular structure and function. Oxidative stress emerges as a common, unifying factor in several conditions including diabetes and cardiovascular diseases. This eBook aims to provide novel data regarding the role played by oxidative stress and inflammation in the development of chronic diseases and the different classes of therapeutics from the bench to the clinic, stressing the awareness of these concepts for the treatment of disease. In addition, articles addressing an overview of the role of oxidative stress in vascular diseases reviewing some current concepts indicating that oxidative stress and inflammation are key mechanisms linking vascular diseases and current state-of-the-art approaches to monitor, prevent and inhibit oxidative stress will be highlighted. There is a close relation between oxidative stress, inflammation and cardiovascular diseases. Despite the great amount of investigation carried out in the field, there are still uncertainties about the mechanisms by which free radicals can modify tissues such as perivascular adipose tissue that ultimately will reflect on vascular function. This eBook will focus on articles that can explore and identify these mechanisms. Concurrent with this understanding of oxidative stress milieu, it is necessary to recognize the need for new pharmacological tools effective in restoring oxidative balance. The abundance of new information and the paradigm shift in our understanding of how antioxidants and other redox-active drugs work in a wide variety of vascular diseases will be specifically highlighted. This eBook will provide a comprehensive, up-to-date source of information on the design and mechanistic, pharmacological, and medicinal aspects of redox-active therapeutics. Finally, a unique feature of the eBook is to provide a way to foster an enthralling discussion revisiting old paradigms and finding new solutions for the treatment of vascular diseases. The topic will include original research articles, hypotheses, perspectives and (mini)reviews from experts in the field. The next decade shows promise for the translation of this body of knowledge to novel human therapeutics and this eBook will enable to increment our knowledge in this field.
Author: Sajal Chakraborti Publisher: Springer Nature ISBN: 9811382735 Category : Science Languages : en Pages : 596
Book Description
This book bridges the gap between fundamental and translational research in the area of heart disease. It describes a multidisciplinary approach, and demonstrates biochemical mechanisms associated with dysregulation of redox signaling, which leads heart disease. Presenting recent studies on improved forms of ROS scavenging enzymes; specific inhibitors for different ROS generating enzymes; and oxidant induced signaling pathways and their antagonists that allow subtle modulation of redox signaling, it also discusses the spatial and temporal aspects of oxidative stress in the cardiovascular system, which are of vital importance in developing better strategies for treating heart disease. Each chapter offers researchers valuable insights into identifying targets for drug development for different types of heart disease.
Author: Sajal Chakraborti Publisher: Springer Nature ISBN: 9811389462 Category : Science Languages : en Pages : 686
Book Description
This book highlights the multifaceted roles of Reactive Oxygen Species (ROS) in modulating normal cellular and molecular mechanisms during the development of different types of heart disease. Each chapter in the book deals with the role that altered redox homeostasis plays in the pathophysiology of heart disease. In addition, the book explains how reactive oxidant species interact with their targets and provides novel strategies for attenuating oxidative stress-induced types of heart disease. The book not only covers ROS-induced response in heart disease at the cellular level, but also demonstrates that an imbalance of redox states has its roots in our genes, and explains the ways gene expression is regulated. In turn, it reviews potential sources of ROS, their pathological effects on the heart, and potential sites for therapeutic interventions.
Author: Martin Rodriguez-Porcel Publisher: Springer ISBN: 1489976930 Category : Science Languages : en Pages : 149
Book Description
This volume explores the role free radicals and antioxidants within the development of vascular disease, examining fundamental research and translating preclinical knowledge to clinical trials. The expertly authored chapters describe the relationship of oxidative stress to atherosclerosis and the cardiovascular system, exploring its role in cardiac fibrosis, renovascular disease, hypertension, and regulation of blood pressure and cerebral vascular tone. The concluding chapter discusses the current state of clinical research, contextualizing clinical trials within the existing theoretical framework and analyzing attempts to preserve oxidant stress under various conditions. With its concise and authoritative analysis of pre-clinical research and clinical results, Studies in Atherosclerosis – part of the bestselling Oxidative Stress in Basic Research and Clinical Practice series – is essential for researchers and clinicians focusing in cardiology, nephrology, or oxidative stress.
Author: Jordan L Holtzman Publisher: Springer Science & Business Media ISBN: 0387723471 Category : Medical Languages : en Pages : 255
Book Description
Vascular injury is initiated by oxidant injury to the vessel wall. This volume is organized around the role of oxidant damage in this disease process and provides a collection of the most recent studies, representing various disciplines that can serve as the basis for further improvements in our understanding and control of cardiovascular and cerebral vascular disease.
Author: Augusto C. Montezano Publisher: Morgan & Claypool Publishers ISBN: 1615043624 Category : Science Languages : en Pages : 105
Book Description
Reactive oxygen species (ROS) influence various physiological processes including host defense, hormone biosynthesis, and cellular signaling. Increased ROS production (oxidative stress) is implicated in many diseases of the cardiovascular system, including hypertension, atherosclerosis, cardiac failure, stroke, diabetes, and kidney disease. ROS are produced throughout the cardiovascular system, in the kidney and central and peripheral nervous system. A major source for cardiovascular, renal, and neural ROS is a family of non-phagocytic NAD(P)H oxidases, including the prototypic Nox2 homologue-based NAD(P)H oxidase, as well as other NAD(P)H oxidases, such as Nox1 and Nox4. Other possible sources include mitochondrial electron transport enzymes, xanthine oxidase, cyclooxygenase, lipoxygenase, and uncoupled nitric oxide synthase (NOS). NAD(P)H oxidase-derived ROS is important in regulating endothelial function and vascular tone and oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in cardiovascular disease. These findings have evoked considerable interest because of the possibilities that therapies targeted against non-phagocytic NAD(P)H oxidase to decrease ROS generation and/or strategies to increase nitric oxide (NO) availability and antioxidants may be useful in minimizing vascular injury and thereby prevent or regress target organ damage associated with hypertension and other cardiovascular diseases.
Author: Qiang Liu Publisher: Frontiers Media SA ISBN: 2832539319 Category : Medical Languages : en Pages : 146
Book Description
Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, pelvis, and kidneys. As a result, different diseases (ischemic heart disease, carotid artery disease, peripheral artery disease, ischemic stroke, and chronic kidney disease) may develop based on which arteries are affected. Atherosclerosis-related diseases are a global crisis and require a global response. The increasing global crisis in atherosclerosis-related diseases is a barrier to development goals including poverty reduction, health equity, economic stability, and human security. There is a synergic action between genetic, ambient, local, and systemic factors, and ultimately the progression of atherosclerosis is responsible for coronary heart disease (CHD) and its complications (such as unstable “in crescendo” angina, myocardial infarction, and sudden death), peripheral arterial disease, and ischemic stroke. Recent investigations show that mitochondrial alterations, oxidative stress and inflammation are inextricably linked and play major roles in the onset and development of atherosclerosis-related diseases. Long-term oxidative stress, autophagy and vascular inflammation could lead to atherosclerosis-related diseases. The evidence of oxidative stress, inflammation, autophagy, mitochondrial dynamic dysfunction, and the interaction of those factors had been proposed.