Phospholipases in Physiology and Pathology presents a comprehensive overview on the physiology and pathology of phospholipases. This seven-volume set considers the biochemical and molecular mechanisms of normal and abnormal cell function upon dysregulation of phospholipases in different diseases. Volumes cover signal transduction mechanisms, implications in cancer, infectious diseases, neural diseases, cardiovascular diseases and other diseases, implications in inflammation, apoptosis, gene expression and non-coding RNAs, the role of natural and synthetic compounds, and stem cell therapies, nanotechnology-based therapies, and more. Together, these volumes give researchers critical insight on the mechanistic and therapeutic aspects of phospholipases.

This book discusses recent advances in our understanding of the role of oxidants in microbial pathophysiology, providing valuable insights into the complex role of reactive oxygen species (ROS) in host-microbial interactions. The various chapters take readers through the function of ROS in infections ranging from viral to bacterial, and describe how microorganisms have developed complex strategies to not only avoid contact with phagocyte-derived oxidants, but also protect themselves from injury when oxidants are encountered. Featuring the latest research in the field of microbial diseases, this timely book is a ready reference for scientists looking to develop new anti-microbial drugs.

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.

Na+-K+ ATPase or Na-pump ATPase, a member of "P"-type ATPase superfamily, is characterized by association of multiple isoforms mainly of it's - and - subunits. At present four different - ( -1, -2, -3 and -4) and three - ( -1, -2, and -3) isoforms have been identified in mammalian cells and their differential expressions are tissue specific. Regulation of Na+-K+ ATPase activity is an important but a complex process, which involves short-term and long-term mechanisms. Short-term regulation of Na+-K+ ATPase is either mediated by changes in intracellular Na+ concentrations that directly affect the Na+-pump activity or by phosphorylation/dephosphorylation-mediated by some stimulants leading to changes in its expression and transport properties. On the other hand, long-term regulation of Na+-K+ ATPase is mediated by hormones, such as mineralocorticoids and thyroid hormones, which cause changes in the transcription of genes of - and - subunits leading to an increased expression in the level of Na+-pump. Several studies have revealed a relatively new type of regulation that involves the association of small, single span membrane proteins with this enzyme. These proteins belong to the FXYD family, the members of which share a common signature sequence encompassing the transmembra ne domain adjacent to the isoform(s) of - subunits of Na+-K+ ATPase. Considering the extraordinary importance of Na+-K+ ATPase in cellular function, several internationally established investigators have contributed their articles in the monograph entitled "Regulation of Membrane Na+-K+ ATPase" for inspiring young scientists and graduate students to enrich their knowledge on the enzyme, and we are sure that this book will soon be considered as a comprehensive scientific literature in the area of Na+-K+ ATPase regulation in health and disease.

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.

This first volume of the comprehensive, two-volume work on oxidative stress in lung disease introduces the molecular mechanisms, and the role of oxidants in the progression of different lung diseases. The lungs of humans and animals are under constant threat from oxidants from either endogenous (e.g. in situ metabolic reactions) or exogenous sources (e.g. air pollutants). Further, oxidative stress causes the oxidation of proteins, DNA and lipids, which in turn generates secondary metabolic products. The book consists of sections, each focusing on different aspects of oxidant-mediated lung diseases. As such it is a unique reference resource for postgraduate students, biomedical researchers and also for the clinicians who are interested in studying and understanding oxidant-mediated lung diseases. The second volume will incorporate other aspects of oxidant-mediated lung diseases, including prevention and therapeutics.

This is the second volume of the comprehensive, two-volume work on oxidative stress in lung diseases. Adopting a multidisciplinary approach, it demonstrates the cellular and molecular mechanisms associated with ROS (reactive oxygen species)-induced initiation and progression of a variety of lung diseases, such as COPD, emphysema, asthma, cystic fibrosis, occupational pulmonary diseases and pulmonary hypertension and discusses points for therapeutic intervention. The book also covers translational research and the latest research on prevention and therapeutics. Each chapter includes in-depth insights into the mechanisms associated with lung diseases and into identifying targets for drug development. Bridging the gap between fundamental and translational research, and examining applications in the biomedical and pharmaceutical industry, it is a thought- provoking read for basic and applied scientists engaged in biomedical research.

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.

Na+-K+ ATPase or Na-pump ATPase, a member of "P"-type ATPase superfamily, is characterized by association of multiple isoforms mainly of it's - and - subunits. At present four different - ( -1, -2, -3 and -4) and three - ( -1, -2, and -3) isoforms have been identified in mammalian cells and their differential expressions are tissue specific. Regulation of Na+-K+ ATPase activity is an important but a complex process, which involves short-term and long-term mechanisms. Short-term regulation of Na+-K+ ATPase is either mediated by changes in intracellular Na+ concentrations that directly affect the Na+-pump activity or by phosphorylation/dephosphorylation-mediated by some stimulants leading to changes in its expression and transport properties. On the other hand, long-term regulation of Na+-K+ ATPase is mediated by hormones, such as mineralocorticoids and thyroid hormones, which cause changes in the transcription of genes of - and - subunits leading to an increased expression in the level of Na+-pump. Several studies have revealed a relatively new type of regulation that involves the association of small, single span membrane proteins with this enzyme. These proteins belong to the FXYD family, the members of which share a common signature sequence encompassing the transmembra ne domain adjacent to the isoform(s) of - subunits of Na+-K+ ATPase. Considering the extraordinary importance of Na+-K+ ATPase in cellular function, several internationally established investigators have contributed their articles in the monograph entitled "Regulation of Membrane Na+-K+ ATPase" for inspiring young scientists and graduate students to enrich their knowledge on the enzyme, and we are sure that this book will soon be considered as a comprehensive scientific literature in the area of Na+-K+ ATPase regulation in health and disease.

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.

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.

In view of rapidly growing research in the deregulation of proteases and their impact in human health and diseases, this book will highlight existing and emerging research in this exciting area. In-depth critical state-of-the-art reviews will be written by established investigators on proteases dysfunctions associated with pathogenesis of different diseases that are known to occur due to deregulation of proteolytic systems. Multidisciplinary approaches demonstrating biochemical and signal transduction mechanisms associated with deregulation of proteases leading to manifestation of the diseases will be discussed. The book highlights the roles of both intracellular and extracellular proteases in health and disease.

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.

This first volume of the comprehensive, two-volume work on oxidative stress in lung disease introduces the molecular mechanisms, and the role of oxidants in the progression of different lung diseases. The lungs of humans and animals are under constant threat from oxidants from either endogenous (e.g. in situ metabolic reactions) or exogenous sources (e.g. air pollutants). Further, oxidative stress causes the oxidation of proteins, DNA and lipids, which in turn generates secondary metabolic products. The book consists of sections, each focusing on different aspects of oxidant-mediated lung diseases. As such it is a unique reference resource for postgraduate students, biomedical researchers and also for the clinicians who are interested in studying and understanding oxidant-mediated lung diseases. The second volume will incorporate other aspects of oxidant-mediated lung diseases, including prevention and therapeutics.

This is the second volume of the comprehensive, two-volume work on oxidative stress in lung diseases. Adopting a multidisciplinary approach, it demonstrates the cellular and molecular mechanisms associated with ROS (reactive oxygen species)-induced initiation and progression of a variety of lung diseases, such as COPD, emphysema, asthma, cystic fibrosis, occupational pulmonary diseases and pulmonary hypertension and discusses points for therapeutic intervention. The book also covers translational research and the latest research on prevention and therapeutics. Each chapter includes in-depth insights into the mechanisms associated with lung diseases and into identifying targets for drug development. Bridging the gap between fundamental and translational research, and examining applications in the biomedical and pharmaceutical industry, it is a thought- provoking read for basic and applied scientists engaged in biomedical research.

This book discusses recent advances in our understanding of the role of oxidants in microbial pathophysiology, providing valuable insights into the complex role of reactive oxygen species (ROS) in host-microbial interactions. The various chapters take readers through the function of ROS in infections ranging from viral to bacterial, and describe how microorganisms have developed complex strategies to not only avoid contact with phagocyte-derived oxidants, but also protect themselves from injury when oxidants are encountered. Featuring the latest research in the field of microbial diseases, this timely book is a ready reference for scientists looking to develop new anti-microbial drugs.

This reference book, which is the second volume of Targeting Oxidative Stress in Cancer, explores oxidative stress as the potential therapeutic target for cancer therapy. The initial chapters discuss the molecular mechanisms of oxidative stress and its effects on different signaling pathways. Subsequently, the sections examine the impact of redox signaling on tumor cell proliferation and consider the therapeutic potential of dietary phytochemicals and nutraceuticals in reactive oxygen species (ROS)-induced cancer. In turn, it examines the evidence supporting the use of Vitamin C in cancer management, before presenting various synthetic and natural compounds that have therapeutic implications for oxidative stress-induced cancer. It also explores the correlation between non-coding RNA and oxidative stress. Furthermore, the book summarizes the role of stem cells in ROS-induced cancer therapy and reviews the therapeutic applications of nanoparticles to alter redox haemostasis in cancer cells. Lastly, it explores heat-shock proteins, ubiquitin ligases, and probiotics as potential therapeutic agents in ROS-mediated cancer. This book is a useful resource for basic and translational scientists as well as clinicians interested in the field of oxidative stress and cancer therapy.

This comprehensive, up-to-date reference work compiles the scientific research on the relationship between various forms of cancer and reactive oxygen species (ROS). It is well known that ROS play a key role in the various steps leading to malignancy, this includes increase in DNA mutation rates. The book brings together exciting reviews, written by leading experts all over the world. The book is divided into four broad sections. Each section describes the role of oxidative stress and underlying mechanisms and pathways, at various stages of cancer, including its role in carcinogenesis, cancer progression and metastasis. Further, the book describes how the reactive oxygen species (ROS) modulate gene expression and signal transduction pathways in cancer. The book discusses the ways to interfere with the cancer progression, and design of anti-cancer drugs. The book provides an integrated approach for better understanding of the development phases of oxidative stress-induced cancers, and mainly the current perspectives about mechanistic aspects of cancer initiation, progression and metastasis. It is a highly resourceful book and would be extremely important to clinicians, students and researchers in the field of cancer genetics, therapeutics and oncology.