Introductory Review on Sirtuins in Biology and Disease provides key insights for scientists and advanced students who need to understand sirtuins and the current research in this field. This book is ideal for pharmaceutical companies as they develop novel targets using sirtuins for metabolic diseases, cancer and neurodegenerative illnesses. Sirtuins are a diverse family of proteins, with several members in mammals. The functional diversity of sirtuins is rather broad, and they have been implicated in various central biological processes. Thus, they are also highly relevant in the context of various human diseases, from cancer to neurodegeneration. - Covers both the general and specific aspects of sirtuin proteins and their role in biology, aging and disease - Presents a top quality collection of leading experts who contribute on a wide range of sirtuin-related topics - Ideal resource for pharmaceutical companies as they develop novel targets using sirtuins for metabolic diseases, cancer and neurodegenerative illnesses

Sirtuin Biology in Cancer and Metabolic Disease: Cellular Pathways for Clinical Discovery offers a compelling and thought-provoking perspective for the examination of the intriguing biology of sirtuins that ties cancer and metabolic disease together and provides a critical platform for the development of sirtuin-based novel therapeutic strategies to effectively treat cancer and metabolic disorders with precision in order to minimize any potentially detrimental clinical outcomes. An exciting prospect for the development of innovative therapeutics for cancer and metabolic disorders involves sirtuins. Sirtuins are histone deacetylases that have an intricate role in the onset and development of cancer and metabolic disease. Implementing a translational medicine format, this innovative reference highlights the ability of sirtuins to oversee critical pathways that involve stem cell maintenance, cellular proliferation, metabolic homeostasis, apoptosis, and autophagy that can impact cellular dysfunction and unchecked cellular growth that can occur during cancer and metabolic disease. Each chapter offers an intuitive perspective of advances on the application of sirtuin pathways for cancer and metabolic disease that will be become a "go-to" resource for a broad audience of scientists, physicians, pharmaceutical industry experts, nutritionists, and students. Chapters are authored by internationally recognized experts who elucidate the intimate relationship between cancer and metabolic disease that intersects with sirtuin pathways Presents the basic and clinical role of sirtuins in regard to cancer and metabolic disease Summarizes the multidiscipline views and publications for this exciting field of sirtuins for the development of new clinical treatments for cancer and metabolic disease Provides a vital foundation for a broad audience of healthcare providers, scientists, drug developers, and students in both clinical and research settings

Sirtuins comprise a family of NAD+-dependent enzymes that have been shown to impact longevity in a number of eukaryotic organisms. Sir2 (Silent Information Regulator 2) was the first sirtuin protein discovered. The discovery that Sir2 requires NAD+ for its activity suggested a link between Sir2 activity and the phenomenon of caloric restriction in prolonging longevity. This link was strengthened by the observation that lifespan extension by caloric restriction requires Sir2 protein. Under conditions of caloric restriction, NAD+ levels are high, Sir2 is activated, and the rate of aging is decreased. These effects have been replicated in invertebrate organisms, where a close structural and functional homologue of Sir2 was found in C. elegans and Drosophila. The sirtuin-dependent effects on metabolism and ageing, observed in lower organisms, have ignited intensive investigation of their biological and therapeutic roles in mammals. There are seven known mammalian sirtuins, SIRTs 1-7, the most studied of which is SIRT1, a close structural and functional homologue of yeast Sir2. Enhancement of organismal longevity and other health-promoting effects of mammalian SIRT1 have frequently been attributed to the regulation of metabolism. A recognized molecular link between metabolism and aging stimulated a firestorm of investigations, aiming to combat metabolic and age-dependent human diseases. It has become clear, however, that the sirtuin family of proteins regulates a diverse repertoire of cellular functions in mammals. Mounting evidence implicating SIRT1 in important clinical indications, such as diabetes, cancer, cardiovascular dysfunction and neurodegenerative disease, suggest that modality as attractive therapeutic target. Subsequently, drug discovery and development, targeting sirtuin activation, has been intensified in the recent years. Despite rapid progress and accumulation of new data, the biological roles of other mammalian sirtuins have been less studied and remain poorly understood. There are several important questions that remain to be addressed. What are the functions of sirtuins in different cell types and tissues? Are all sirtuins involved in the regulation of metabolism and aging? What is the functional relationship between different sirtuins? What are the mechanisms of regulation of sirtuin activities? What is the role of sirtuins in disease and therapy? This issue aims to address these and other critical questions, relevant to Research Topic on sirtuin biology and therapeutics. To that end the issue solicits expert opinions of sirtuin research on structural biology, biochemistry, cell biology, animal genetics, pharmacology, medicinal chemistry and drug discovery, and on areas of investigation studying human conditions, like diabetes, cancer, cardio-vascular, and neutodegeneration. Of particular interest are the new methods and assays to study sirtuins in various organisms and developing sirtuin-based therapeutics. Furthermore, we propose to encourage contributors to discuss new concepts and paradigms, and to express their perspectives on the future development of the sirtuin research field. Altogether, we believe this issue provides a unique opportunity for comprehensive and diverse coverage of the topic, and will be of broad interest for the journal’s readership.

The book highlights work from many different labs that taught us abnormal HDACs potentially contribute to the development or progression of many human diseases including immune dysfunctions, heart disease, cancer, memory impairment, aging, and metabolic disorders.

Recent studies have indicated that epigenetic processes may play a major role in both cellular and organismal aging. These epigenetic processes include not only DNA methylation and histone modifications, but also extend to many other epigenetic mediators such as the polycomb group proteins, chromosomal position effects, and noncoding RNA. The topics of this book range from fundamental changes in DNA methylation in aging to the most recent research on intervention into epigenetic modifications to modulate the aging process. The major topics of epigenetics and aging covered in this book are: 1) DNA methylation and histone modifications in aging; 2) Other epigenetic processes and aging; 3) Impact of epigenetics on aging; 4) Epigenetics of age-related diseases; 5) Epigenetic interventions and aging: and 6) Future directions in epigenetic aging research. The most studied of epigenetic processes, DNA methylation, has been associated with cellular aging and aging of organisms for many years. It is now apparent that both global and gene-specific alterations occur not only in DNA methylation during aging, but also in several histone alterations. Many epigenetic alterations can have an impact on aging processes such as stem cell aging, control of telomerase, modifications of telomeres, and epigenetic drift can impact the aging process as evident in the recent studies of aging monozygotic twins. Numerous age-related diseases are affected by epigenetic mechanisms. For example, recent studies have shown that DNA methylation is altered in Alzheimer’s disease and autoimmunity. Other prevalent diseases that have been associated with age-related epigenetic changes include cancer and diabetes. Paternal age and epigenetic changes appear to have an effect on schizophrenia and epigenetic silencing has been associated with several of the progeroid syndromes of premature aging. Moreover, the impact of dietary or drug intervention into epigenetic processes as they affect normal aging or age-related diseases is becoming increasingly feasible.

The focus of this collection of illustrated reviews is to discuss the systems biology of free radicals and anti-oxidants. Free radical induced cellular damage in a variety of tissues and organs is reviewed, with detailed discussion of molecular and cellular mechanisms. The collection is aimed at those new to the field, as well as clinicians and scientists with long standing interests in free radical biology. A feature of this collection is that the material also brings insights into various diseases where free radicals are thought to play a role. There is extensive discussion of the success and limitations of the use of antioxidants in several clinical settings.

This multivolume reference work addresses the fact that the well being of humankind is predicated not only on individuals receiving adequate nutrition but also on their genetic makeup. The work includes more than 100 chapters organized in the following major sections: Introduction and Overview; Epigenetics of Organs and Diseases in Relation to Diet and Nutrition; Detailed Processes in Epigenetics of Diet and Nutrition; Modulating Epigenetics with Diet and Nutrition; and Practical Techniques. While it is well known that genes may encode proteins responsible for structural and dynamic components, there is an increasing body of evidence to suggest that nutrition itself may alter the way in which genes are expressed via the process of epigenetics. This is where chemically imposed alteration in the DNA sequence occurs or where the functional expression of DNA is modulated. This may include changes in DNA methylation, non-coding RNA, chromatin, histone acetylation or methylation, and genomic imprinting. Knowledge regarding the number of dietary components that impact on epigenetic processes is increasing almost daily. Marshalling all the information on the complex relationships between diet, nutrition, and epigenetic processes is somewhat difficult due to the wide myriad of material. It is for this reason that the present work has been compiled.