Current evidence suggests that the ischemic preconditioning response is a multi-factorial process consisting of an initial early trigger, an intermediate mediator, and an end effector. Each of these steps in is now its own intense area of investigation. The need to render the heart ischemic for a brief period to invoke the preconditioning response is currently the major factor limiting clinical application of this powerful cardioprotective strategy. Recent research efforts have utilized brief exposures to pharmacological agents, in lieu of a brief preconditioning ischemia, to trigger/mimic the ischemic preconditioning-induced response. The World Heart Congress held in Winnipeg in July 2001 provided a forum for the presentation of new insights into the basic mechanisms of ischemia and reperfusion injury, as well as novel strategies to protect the heart from cell death, ventricular arrhythmias, and contractile dysfunction. Many pioneers in the fields of ischemia-reperfusion injury and preconditioning-induced protection presented there and the chapters in this book represent selected papers from these symposia.

According to the World Health Report (2000 http:/ /www. who. int/whr), of the 55 million deaths worldwide in 1999, more than 16 million were secondary to car diovascular complications. With the prospect of world population increasing from the current level of 6 billion to 9 billion by the middle of this century, the burden of cardiac disease is going to increase astronomically. Furthermore, scientists are being challenged not only to reduce mortality, but also to improve quality of life. Thus, more than ever, intellectuals from different disciplines including biology, sociology, informatics and health care have to join forces to meet the mandate. The World Heart Congress with a focus on "Frontiers in Cardiovascular Health" held in Winnipeg during July 6-11, 2001, made a unique attempt to bring these specialists together to brainstorm and map out the course of action for cardiovascular research and health in the next century. Anytime there is a relative increase in the workload on the heart, there are adap tive myocardial as well as humoral responses. When these adaptations or remodel ing at the organ, subcellular or gene level, become inadequate for a proper tissue perfusion, the condition of heart failure ensues. Prevention of the factors leading to the relative increase in workload as well as a better understanding of the adap tive responses and their failure are some of the hopes to combat the morbidity and mortality due to heart failure.

Mechanisms of Heart Failure is based on papers selected from poster presentations made at the International Conference on Heart Failure, Winnipeg, May 20-23, 1994. Although the entire book is one continuous discussion of subcellular mechanisms of heart failure and its treatment, the presentation has been divided into three sections: the opening section on the subcellular basis of heart failure includes discussions of cytokines, signal transduction, metabolism, extracellular matrix, organ level changes and newer approaches to understanding the pathogenesis of heart failure. The second section focuses on the pathophysiological aspects of cardiomyopathies and their treatment. In the final section, medical, surgical and pharmacological approaches to the treatment of heart failure are discussed in clinical and animal laboratory settings.

This monograph contains 20 selected papers presented at the Symposium on Subcellular Basis of Contractile Failure which was held in Ottawa during May 11-13, 1989 and is designed for the benefit ofthose who were unable to attend this event. It is now increasingly becoming clear that an excessive amount of calcium is intimately involved in the pathogenesis of a wide variety of heart diseases. Accordingly, the investigations concerning the role of calcium chan nels and their regulatory mechanisms in heart function as well as of the intra cellular calcium overload in cardiac dysfunction are presented here. Since sodium is also considered to influence the cardiac contractile force by chang 2 ing the intracellular concentration of calcium through the Na +-Ca+ exchange 2 mechanism in the cell membrane, the role of Na +-Ca+ exchange in heart func tion as well as pathology of contractile failure is discussed. In view of the new ly discovered implications of the oxygen free radicals in cellular injury, papers concerning the role of these radicals in heart disease are included in this book. For the purpose of clarity, different chapters have been organized under three main headings: (I) Role of cations in heart function, (II) Cardiac hypertrophy and cardiomyopathies, and (III) Ischemic heart disease and cardiac failure."

Heart Hypertrophy and Failure brings together leading basic scientists and clinicians, presenting improved knowledge of the pathophysiology and treatment of the condition. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system in health and disease. The papers presented describe fundamental mechanisms underlying changes in the cellular machinery during the development of cardiac hypertrophy and heart failure. Audience: Students, scientists, clinical and experimental cardiologists who seek to understand and manage the perplexing problems of hypertrophy and heart failure.

Pathophysiology of Heart Failure brings together leading basic scientists and clinicians, presenting new approaches to this complex problem, involving cardiomyopathic processes and ischemia perfusion injury. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system. The role which excess intracellular calcium plays in the genesis of cardiac dysfunction is described as a fundamental mechanism underlying heart failure; one which may lead to improved prevention and treatment. Audience: Clinical and experimental cardiologists will find the book a helpful source of ideas and inspiration.

Proteases form one of the largest and most diverse families of enzymes known. Once considered primarily as "enzymes of digestion," it is now clear that proteases are involved in every aspect of cellular function. Members of the diverse families of proteases act to promote cellular proteolysis found in nature, and their deregulation may result in different pathophysiological conditions, such as tumor progression, vascular remodeling, atherosclerotic plaque progression, ulcer, rheumatoid arthritis, and Alzheimer's disease. Many micro-organisms require proteases for replication or use proteases as virulence factors, which have facilitated the development of protease-targeted therapies for a variety of parasitic diseases. Proteases in Health and Disease represents a comprehensive overview of the fascinating field of proteases by various renowned experts, and focuses on the recently elucidated functions of complex proteolytic systems in physiology and pathophysiology. Part A, Molecular and Biochemical Aspects of Proteases, illustrates some of the major proteases, such as calpains, matrix metalloproteases, fibrinolytic serine proteases, and aspartic proteases, which play a significant role in a variety of pathologies and may be a target for therapy either by their up regulation or down regulation. Part B, Involvement of Proteases in Diseases Processes, deals with the functional roles of the individual proteases in the progression of diseases such as cardiovascular and inflammatory lung disease, malaria, cholera, autism spectrum disorder, hepatitis, and ischemia-reperfusion injury induced cardiac diseases. With this multi-disciplinary scope, the book bridges the gap between fundamental research and biomedical and pharmaceutical applications, making this a thought-provoking reading for basic and applied scientists engaged in biomedical research.

Pathophysiology of Cardiovascular Disease has been divided into four sections that focus on heart dysfunction and its associated characteristics (hypertrophy, cardiomyopathy and failure); vascular dysfunction and disease; ischemic heart disease; and novel therapeutic interventions.
This volume is a compendium of different approaches to understanding cardiovascular disease and identifying the proteins, pathways and processes that impact it.

In 1982, as chance would have it again, an opportunity appeared to Jom the Department of Physiology at Kuwait University. P. Braveny spend four years there, teaching, doing some research, recovering former international contacts. Coming back home, he faced the same gloomy, motionless disfavor as before. November 1989 turned P. Bravenfs career upside down. Immediately after the fall ofthe communist regime, he was elected vice-dean and later dean ofthe Faculty of Medicine, promoted full professor in physiology and appointed the head of the Department ofPhysiology. From 1992 to 1998 P. Braveny served as the vice-rector of Masaryk University. His professional career culminated in his presidency of the XIV World Congress of ISHR in Prague. Understandably, in the following years, he become interested (in his tutor's footsteps) in history of physiology and pub- lished two monoghaphs (E. Babak andV Kruta). This CV would be an incomplete one without mentioning his broad interests in natural sciences and in art, particu- larly music and painting. As a tutored amateur he has acquired certain success in the latter. When reviewing P. Bravenfs whole-life work, largely done under adverse cir- cumstances with minimum financial support, his almost two hundred papers, innu- merable essays and four monographs are a commensurate result. In appreciation, he was awarded honorary membership of the Czech Medical Society, Physiological Society and Cardiological Society, Gold Medal of Masaryk University, Ministry of Education Award etc. Bohuslav Ostadal Makoto Nagano Naranjan S.

The Frontiers in Cardiovascular Health varies between and within nations, depend ing upon the level at which the battle is fought for better cardiovascular health. According to the 1997 World Health Report, 15 million deaths (i. e. 30% of the total number of deaths) were attributable to cardiovascular diseases and this number is on the rise. The projection for the year 2020 is quite alarming with an expected cardiovascular mortality reaching 50 million. Much of this burden is projected to occur in developing countries, more specifically in the most populous countries of the world, namely China and India. These countries are already burdened with infectious and parasitic diseases and are trying to eradicate such diseases. With increasing life expectancies people all over the world, especially in developing coun tries, are exposed to degenerative atherosclerosis resulting in increased cardiovascu lar mortality and morbidity. In developing countries, resources available for health care are very limited. For example many of the African countries spend less than $10 per person per year on his/her entire health care let alone cardiovascular health. The average health care budget for nearly two thirds of the global population is well below $100 per year, on a per capita basis. Therefore, in developing countries health promotion and primary prevention are the frontiers by necessity. Improving awareness and health education is not only a matter of choice but is an absolute necessity.

Research at the molecular and the cellular level has greatly enhanced our understanding of the pathogenesis and management of heart disease. Valuable contributions, towards this end, have been made by scientists from different dis ciplines including biochemistry, physiology, pathology, molecular biology and biophysics. We felt that it would be of interest and value to bring together ex perts from diverse specialities to present their work and to discuss the common problems encountered in their endeavours. In accordance, a symposium was organised in February 1988 at the Postgraduate Institute of Medical Education & Research, Chandigarh. It was held during the annual meeting of the Indian section of the International Society for Heart Research. This book is a compila tion of some of the papers presented at the symposium. The symposium was sponsored by the Council on Cardiac Metabolism of the International Society and Federation of Cardiology. A number of Indian or ganisations gave generous financial help. These included the National Academy of Medical Sciences, Indian Council of Medical Research, Council of Scientific and Industrial Research and Department of Science and Technology. Desktop publishing was used to prepare this volume. In doing so we came to appreciate the remarkable qualities, skills and help rendered by Professor Dharam Vir. For typing the manuscripts and for other secretarial assistance we gratefully acknowledge the help of Ravinder and Sawtantar. PATHOPHYSIOLOGY AND PHARMACOLOGY OF HEART DISEASE 1 THE NEWBORN PIG HEART, A SUPERIOR ANIMAL MODEL OF CARDIAC HYPERTROPHY Howard E."

The importance of heart and artery disease as a cause of death and disability is difficult to exaggerate: it causes over half of all deaths in the western world and now accounts for one-quarter of deaths in the entire world. This appalling incidence persists in spite of commendable progress in treatment and prevention, particularly in the last two or three decades. Deaths from coronary disease have decreased by a third in the past twenty years and stroke has decreased by a half in the same period. This remarkable improvement, saving thousands of lives per year, has come about due to changes in life style (low fat diet, control of high blood pressure, less smoking and more exercise) and progress in treatment (more effective drugs, coronary care units, pacemakers, and cardiac surgery). Progress in understanding the pathophysiologic and pharn, acologic mechanisms operative in heart disease have been paramount in the development of more rational and more effective therapy. Dramatic and spectacular surgical treatments have fired the public imagination. Bypass surgery is commonplace and results in complete or considerable relief of symptoms in the majority of patients operated upon

In the course of the last two decades, it has become increasingly evident that the sarcolemmal, sarcoplasmic reticular and mitochondrial membrane systems play an important role in determining the status of heart funotion in health and disease. These organelles have been shown to be intimately involved in the regulation of cation movements during the contraotion-relaxation cycle. Various proteins imbedded in the phospholipid 2+ + - + + bilayers of these membranes control Ca, Na, Cl, K and H concentrations within the oytoplasm by indirect or direct means. Cationic channels, Na+, + 2+ 2+ 2+ + 2+ + + K -ATPase, Ca IMg ATPase, Ca pump, Na -Ca exchanger, Na -II exchanger and adenylate cyclase affect myocardial funotion and viability through their role as regulators of specific ion movements. However, proteins are not the only important constituents of the membrane. Any disturbance in the interaction between proteins and phospholipids in the membrane has been suggested to alter the funotion of the organelles, upset ionic homeostasis and precipitate the development of abnormalities in oardiac performance. It is, therefore, orucial to understand the faotors whioh regulate membrane funotion in their totality if we are to oomprehend the nature of heart performanoe in healthy subjects. Similarly, the study of membrane dysfunotion in a wide variety of experimental models of heart disease at various stages of failure is essential if we are to fully understand the pathogenesis of heart dysfunotion and improve its treatment.

It is indeed ironical that in the absence of a complete knowledge of Pathophysiology, clinical cardiologists are left with no choice but to do the best they can to help the patient with the armamentarium of drugs at their disposal. But nothing could be further from truth than to treat the diagnosed end point of a disease process without a full understanding of its patho physiology. This point was eloquently made by Dr. Arnold Katz in his Presidential Address (Chapter 1) at the 8th Annual Meeting of the American Section of the International Society for Heart Research held in Winnipeg, Canada, July 8-11, 1986. This volume represents a part of the scientific proceedings of this Meeting. From a reading of this treatise it will become evident that discoveries of newer scientific facts as well as a better understanding of pathophysiology are continuously influencing/ improving our therapeutic approaches in modern medicine. In this book, latest biochemical, physiological and pharmacological findings on different experimental models such as Myocaridal hypertrophy, Hypertension and heart failure, Diabetes, Cardio myopathies and Cardiac function in shock are described by internationally recognised experts. Hopefully information presented here will provide another building block to the edifice of Science of Cardiology which we all are trying to create. Acknowledgements We are grateful to the following Agencies and Foundations for their generous financial support of the Symposium, which formed the basis of this book. A. Major Contributors: 1. Manitoba Heart Foundation 2. Sterling-Winthrop Research Institute 3. Squibb Canada, Inc."

Molecular Defects in Cardiovascular Diseaseprovides an in-depth discussion of the molecular mechanisms underlying the genesis of cardiovascular defects and the implications this has on current and emerging targeted therapeutics. Divided into three sections, this book covers the scientific foundations of our present understanding as well as the array of clinical manifestations and their treatment. The first section covers Molecular Mechanisms of Heart Disease, with discussion of the development of cardiovascular dysfunction. The remaining two sections provide a more clinical focus. The second, Cardiac Hypertrophy and Heart Failure deals with metabolic derangements, Ca2+ handling, and subcellular remodeling. It illustrates the wide variety of molecular defects which may serve as targets associated with the transition from cardiac hypertrophy to advanced heart failure. The third section, Hypertension and Diabetes, provides molecular rationale for the pathogenesis of hypertension and diabetic cardiomyopathy, as well as highlighting the importance of hormones toward this end.

A necessary resource for clinicians and researchers, this book elucidates the experimental basis of the practice of cardiology. It is the culmination of our advances in the understanding of cardiovascular molecular biology and a blueprint for the efficacious use of targeted therapies.

The relationship between angiotensin II and hypertension was established in 1898 when angiotensin II was shown to modulate systemic blood pressure. Over the intervening decades, a complete characterization of the renin-angiotensin system (RAS) has been achieved, and our understanding of its biochemistry and physiology has led to the directed development of agents such as ACE inhibitors and receptor antagonists capable of controlling hypertension. More recently, it was shown that angiotensin II is secreted within certain tissues, and that these tissue-specific systems operate independently of the systemic RAS. The novel concept that angiotensin II regulates a number of cardiovascular processes that are unrelated to blood pressure has renewed the interest of both basic and clinical scientists in angiotensin II. The association between angiotensin II and cardiac growth, in particular, has indicated that therapies currently in use for hypertension may have direct application to the treatment of heart failure. Angiotensin II Receptor Blockade: Physiological and Clinical Implications focuses on the most recent developments in the molecular biology, cellular physiology and structure-function relationships of angiotensin II and its receptors. In addition, this volume covers the current therapeutic uses for angiotensin receptor antagonists and considers their potential future applications. This volume will be a valuable resource for scientists, practising clinicians and students who are attempting to extend their knowledge in the field of hypertension and heart failure, and who are devoted to improving cardiovascular health.

In an attempt to clarify the situation regarding the diagnosis, pathogenesis and therapeutics of cardiovascular dysfunction in diabetes, an International Symposium on Diabetic Heart was held in Tokyo, Japan during October, 1989. Thirty-two selected articles from the poster presentations, compiled in this book, have been grouped in four sections, namely (a) Evaluation of Cardiovascular Problems, (b) Interactions of Diabetes and Hypertension, (c) Pathophysiological Aspects of Cardiovascular Dysfunction in Diabetes, and (d) Pharmacological and Therapeutic Aspects of Diabetic Heart. It is hoped that the contents of these chapters will provide adequate information regarding the current status of cardiovascular abnormalities in diabetes and this book will be of great interest to both clinical and experimental cardiologists as well as endocrinologists interested in diabetes.

As the majority of cardiovascular deaths are related to myocardial ischemia, it is necessary to understand the various aspects of ischemic heart disease. In this regard, it is noteworthy that ischemic heart disease is commonly associated with atherosclerosis, coronary spasm, as well as thrombosis leading to the development of arrhythmias, cardiovascular cell damage, myocardial infarction, cardiac hypertrophy and congestive heart failure. Furthermore, it is also important to appreciate various physiological, electrophysiological and biochemical processes in the normal heart if we are to understand their significance under pathological situations. Heart Function in Health and Disease has been organized in five sections to provide an outline of a complex problem in a convenient manner. One section of this book is devoted to shedding light on the restructuring and ontogenic changes in the developing heart whereas in the next section some hypertrophic alterations due to chronic hypoxia are described. The third and fourth sections of this book are concerned with the regulation of cardiac channels as well as signal transduction mechanisms and cardiac electric field. The fifth section contains some pathophysiological events during the development of cardiac hypertrophy and heart failure. All of these areas encompass a significant body of new information that will be invaluable to those who work in the field of cardiovascular sciences, as well as those who treat people with heart disease.

Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid linked signal transduction pathways are activated in some specific manner depend ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.

Diabetes and cardiovascular disease together account for the largest portion of health care spending compared to all other diseases in Western society. This work seeks to provide an understanding of the causes of diabetes and its cardiovascular complications. As this understanding becomes more widely appreciated, it will serve as a foundation for evidence-based care and wider acceptance of sound science. The International Conference on Diabetes and Cardiovascular Disease, held in Winnipeg, in June 1999, was organized to bring together a multi-disciplinary group of researchers dedicated to further knowledge amongst researchers, care givers, and the managers of the health system. The invited speakers submitted their works for publication, which serves as the basis for this book. Major themes include: epidemiology of diabetes mellitus, metabolic risk factors in diabetes and cardiovascular disease, hypertension in diabetes mellitus, cardiac function in diabetes, glycemic control and improved cardiovascular function, diabetes management, and endothelial function in diabetes.

Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor mation is beginning to provide tangible targets towards manipulating cardiac func tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben eficial response under many conditions, it can be highly deleterious and inappropri ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben eficial."

This book, which is the third volume of Biomedical translational research, focuses on the fundamental role of biomedical research in developing new medicinal products. It emphasizes the importance of understanding biological and pathophysiological mechanisms underlying the disease to discover and develop new biological agents. The book uniquely explores the genomic computational integrative approach for drug repositioning. Further, it discusses the health benefits of nutraceuticals and their application in human diseases. Further, the book comprehensively reviews different computational approaches that employ GWAS data to guide drug repositioning. Finally, it summarizes the major challenges in drug development and the strategies for the rational design of the next generation more effective but less toxic therapeutic agents.

A recent comprehensive study of stress and human health by the Institute of Medicine/National Academy of Sciences concludes that individuals who experience any of a wide range of stressful events or situations are at increased risk of developing a physical or mental disorder, including heart disease. Since cardiovascular disease continues to be a leading cause of illness and death, and since the etiology and pathogenesis of several of the commonest forms of heart disease are incompletely known, it is of fundamental impor tance to study the potential role of stress in the genesis of heart disease. Accordingly an International Symposium on Stress and Heart Disease was held in Winnipeg, Canada, June 26-29, 1984 and the proceedings form the basis of this book and its companion volume, "Stress and Heart Disease." The connection between stress (the behavioral sciences) and heart disease (the biomedical sciences) occurs in the mechanisms through which the brain affects or controls the endocrine and the autonomic nervous systems. Initially this linkage appeared to be relatively simple, mainly involving catecholamines and corticosteroids, and communication between nerve cells was thought to be electrical. Now knowledge has increased and concepts have change dramatic ally. Major advances have occurred in biochemical, anatomical, physiological, pharmacological, pathological and behavioral aspects of the neuroendocrine system. The over whelming significance of chemical communication in the nli xviii nervous system has become clear."

It is now well known that proteases are found everywhere, in viruses and bacteria as well as in all human, animal and plant cells, and play a role in a variety of biological functions ranging from digestion, fertilization, development to senescence and death. Under physiological conditions the ability of proteases is regulated by endogenous inhibitors. However, when the activity of proteases is not regulated appropriately, disease processes can result, as seen in Alzheimer s disease, cancer metastasis and tumor progression, inflammation and atherosclerosis. Thus it is evident that there is an absolute need for a tighter control of proteolytic activities in different cells and tissues.

Aimed at graduate students and researchers with an interest in cellular proteolytic events, "Role of Proteases in Cellular Dysfunctions" is the second book on Proteases in this series. The book consists of three parts in specified topics based on current literatures for a better understanding for the readers with respect to their subject-wise interests. The first section of this book covers a brief idea about the neuronal disorders and the involvement of proteases such as calpains, caspases and matrix metalloproteases (MMPs). The second section covers the deadly disease cancer and its relation to ubiquitin-proteasome system, MMPs and serine proteases. The last section is about the role of proteases such as calpains, MMPs and serine protease as well as urokinase type plasminogen activator receptor (uPAR) in causing cardiovascular defects. "

The biological membranes of cellular organization enfold an important group of membrane proteins called the ATPases, which are not only versatile in maintaining chemical gradient and electrical potential across the membrane but also bring metabolites necessary for cell metabolism and drive out toxins, waste products and solutes that otherwise can curb cell functions. ATPases are distributed virtually in all live forms starting from unicellular to multicellular and also in viruses. There are different types of ATPases, which differ in function and structure and in the type of ions they transport. The three main types of the ion pump ATPase family are: (i) P-type ATPases that transport different ions across membranes and Ca2+ATPases belongs to this catagory (ii) F-type ATPase in mitochondria, chloroplasts and bacterial plasma membranes produce ATP using the proton gradient; and (iii) V-type ATPase catalyzes ATP hydrolysis to transport solutes and maintains acidic pH in organelles like lysosomes. Genetic defects in either of the ATPases cause several diseases and a number of researches have demonstrated the involvement of the members of ATPases in the cell pathology and diseases, thereby penetrating exciting new areas of our understanding. In this book, the authors summarize recent knowledge about the molecular mechanisms associated with Ca2+-ATPase, V-ATPase and F-ATPase in intracellular and extracellular Ca2+ transport, mitochondrial ATP synthase, vesicular H+ transport, and lysosomal pH regulation. This book thereby bridges the gap between fundamental research and biomedical and pharmaceutical applications. The book provides an informative resource to improve ATPase research and modern therapeutic approaches toward different life threatening diseases that are associated with dysregulation of the ATPases.