Biochemistry Of Atherosclerosis

This book covers many aspects of atherogenesis, with particular emphasis on lipid and lipoprotein metabolism. It includes all aspects of the regulation of cholesterol homeostasis and the importance of each pathway. Also explored are the roles of nuclear hormone receptors on lipid and lipoprotein metabolism and their complex roles in atherogenesis. The book further discusses how genetic studies can help understand the complexities that mediate these aspects of atherogenesis.

In this first full-length review of the biochemical parameters and their part in the pathogenesis of atherosclerosis, the reader will discover a range of coverage concerning basic etiological factors and the relationship between the biochemistry of the disease and its clinical manifestations. The book begins with an authoritative overview of lipoprotein structure, metabolism, and quantification, including a critical analysis of the most important techniques utilized in these studies. The focus then moves to the metabolic events attending the interaction of serum lipoprotein with cells and also the functional activities of the arterial wall and how these reactions are regulated.

Diabetes is an autoimmune, inflammatory disease affecting many different organ systems and exhibiting both primary and secondary defects. Because diabetes affects a wide range of cellular systems, a multidisciplinary effort has been mounted over the past several decades using a wide range of investigative techniques and methodologies in order to identify molecular mechanisms responsible for cellular dysfunction. Because primary defects at various levels of sub-cellular signaling, intracellular calcium handling, protein expression and energy regulation are often a primary consequence of diabetes. This volume is a compilation of new multidisciplinary research that will broaden our current understanding of diabetes and cardiovascular disease as well as provide the basis for the development of novel therapeutic interventions.

Atherosclerotic cardiovascular disease remains the major cause of death and disability in Western society. The field of atherosclerosis research has grown tremendously over the last forty years, shedding a great deal of light on the contributing factors and natural history of the disorder and enabling strategies for its treatment and prevention. Some of the greatest strides in this field in recent years have derived from advances in molecular biology techniques. These strides were chosen for emphasis in the most recent Princess Lilian symposium, whose proceedings this volume represents. Historically, the Princess Lilian meetings have been small ones aimed at bringing together investigators from diverse specialties to discuss a particular subject. The most recent meeting was no exception and included clinicians, clinical investigators, and research ers in basic science. The symposium began with an extensive review of coronary morphopathological findings in patients who died of coronary heart disease. Any rational hypothesis of atherogenesis must take into account clinical findings, and any attempt to bridge the gap between experimental laboratory findings and studies in man is highly desirable. Three chapters focus on endothelial injury: one on the nitric oxide pathway in physiology and pathology, a second on the activation of endothelial cells, and a third on the monocyte and endothelial injury. Still another chapter examines growth factors, in particular the fibroblast growth factor in atherogenesis.

New discoveries in genetics, molecular, and cell biology are not only enhancing our understanding of the etiology and progression of disease, but are finding applications in the development of new drugs or the implementation of new kinds of therapy. This book provides an in-depth review of emerging areas in biomedical research at the interface of s

Age is a nonreversible risk factor for atherosclerosis. The atherosclerotic process begins early in life, progresses during the middle years, and usually culminates in clinical disease towards the later years of the life span. Since atherosclerosis is a multifactorial disease, and many of the "risk factors" are time- and age related, it has been difficult to sort out intrinsic aging from environmental factors that operate over many years. Furthermore, the role of genetic factors remains unknown. This workshop has produced much worthwhile information that is helping elucidate the impact of age on atherogenesis. Important strides have been made in understanding the role of changes in the arterial wall and of lipoproteins, platelets, and monocyte-derived macrophages in the disease process. In parallel, our understanding of the biology of aging has increased sufficiently so that these two areas of interest can now profitably intersect. The proceedings of this successful workshop emphasize that there is much to be gained by continued interaction between those scientists interested in the biology of aging at all levels and those interested in the atherosclerotic process. Hopefully, we may eventually progress in our understanding and reach the stage when atherosclerosis will no longer be an inexorable concomitant of human aging. Edwin L. Bierman, M. D. Contents Foreword V Contributors IX Participants in the Workshop XV Introduction and Statement of Research Recommendations Sandra R.