This volume reviews available mouse models of atherosclerosis, basic aspects of disease initiation and progression, and the visualization of atherosclerotic lesions with invasive and non-invasive techniques that are widely used both in basic research and in the clinic. The chapters catalogue a wide range of in vitro and in vivo experimental methods used for atherosclerosis research, including thorough protocols and valuable notes based on the authors’ personal wet lab experience. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls. Authoritative and practical, Methods in Mouse Atherosclerosis will be a valuable working guide for researchers performing mouse-based atherosclerosis studies.

Angiogenesis and Cardiovascular Disease provides a comprehensive review of the basic scientific and clinical advances in the field of angiogenesis, and its role in the human cardiovascular system. The material presented draws from multiple disciplines, integrating information in a single source. Topics addressed focus first on aspects of development and normal biology of the vasculature, and then on angiogenesis and how it is involved in the pathophysiology and therapy of ischemic cardiovascular disease. Vascular development, endothelial cell biology, the vascular matrix, and growth factors are discussed. Up to date information on current clinical trials, and practical advice concerning application to cardiovascular therapeutic options, are also stressed.

This book is a methodological source on mice models of vascular diseases. Covering various areas, each chapter is written by a pioneering researcher who has developed an original vascular disease model. Notoriously difficult to reproduce, each model is described in detail and numerous photographs are provided with links to videos. Genetically modified mice are a very powerful tool for studying the pathogenesis of various diseases, including immunological and oncological disorders, but they had always been thought to be too small to be used in the field of cardiovascular disease. Recently, however, various mice models of vascular diseases have been reported, and these will make a substantial contribution to basic research on cardiovascular and metabolic disorders.

New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.

The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation. Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References

Research centering on blood flow in the heart continues to hold an important position, especially since a better understanding of the subject may help reduce the incidence of coronary arterial disease and heart attacks. This book summarizes recent advances in the field; it is the product of fruitful cooperation among international scientists who met in Japan in May, 1990 to discuss the regulation of coronary blood flow.

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.