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This book describes current methods for the identification and characterization of the major hallmarks of senescent cells. Chapters focus on the high heterogeneity of the senescence phenotypes, and techniques to induce and identify specific senescence programs. Additional chapters describe cellular and mouse models in which is possible to study the complex cell and non-cell autonomous functions of senescent cells. 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 tips on troubleshooting and avoiding known pitfalls. Authoritative and cutting-edge, Cellular Senescence: Methods and Protocols aims to ensure successful results in the further study of this vital field.
Cellular Ageing and Replicative Senescence by Suresh I.S. Rattan,Leonard Hayflick Pdf
This book covers the origins and subsequent history of research results in which attempts have been made to clarify issues related to cellular ageing, senescence, and age-related pathologies including cancer. Cellular Ageing and Replicative Senescence revisits more than fifty-five years of research based on the discovery that cultured normal cells are mortal and the interpretation that this phenomenon is associated with the origins of ageing. The mortality of normal cells and the immortality of cancer cells were also reported to have in vivo counterparts. Thus began the field of cytogerontology. Cellular Ageing and Replicative Senescence is organized into five sections: history and origins; serial passaging and progressive ageing; cell cycle arrest and senescence; system modulation; and recapitulation and future expectations. These issues are discussed by leading thinkers and researchers in biogerontology and cytogerontology. This collection of articles provides state-of-the-art information, and will encourage students, teachers, health care professionals and others interested in the biology of ageing to explore the fascinating and challenging question of why and how our cells age, and what can and cannot be done about it.
Cellular Senescence in Disease by Manuel Serrano,Daniel Munoz-Espin Pdf
Winner of the 2023 PROSE award in Biomedicine and Neuroscience! Research in the field of senescence has boomed recently due to the gradual realization that senescent cells are associated with a significant number of diseases. The genetic or pharmacological elimination of senescent cells can cause widespread benefits and improves outcomes for most of those diseases. Cellular Senescence in Diseases presents an updated review of the role of cellular senescence in multiple pathologies. Focus is given to those diseases where the implication of senescence has been more extensively documented, such as (cancer, lung and liver diseases, diabetes, Neurodegenerative diseases and others). The Editors recruited a group of worldwide experts in each individual pathology to review the role of cellular senescence in each one of them, aiming at identifying potential therapeutic pathways. The first two chapters provide an overview of the cellular senescence principles. Next, the chapters are divided into specific diseases. Cancer, including premalignant lesions (OIS), Advanced disease (TIS), and Metastasis are covered. The following condition covered is Lund diseases, including IPF, COPD, and Pulmonary Hypertension. Next Liver Diseases are covered, including Fibrosis and Cirrhosis, and Fatty liver disease. Next there is coverage for Kidney implications, including fibrosis and transplantation. Vascular diseases are covered next including infarction and hear fibrosis, and atherosclerosis. Both diabetes types 1 and 2 are covered next. Following chapters cover Obesity, Sarcopenia, and Bone and Cartilage disorders, respectively. Neurodegenerative diseases are covered next, focusing on Alzheimer and Parkinson. The next chapter discusses accumulation of senescent cell in tissues during aging. The two final chapters cover current developments and conclusions. Cellular Senescence in Diseases is designed for researchers and clinicians with a focus on the cellular mechanisms of diseases. All chapters cover current experimental therapeutic approaches to eliminate or cancel the pathological effects of senescent cells. Pharmaceutical scientists may also benefit from the contents of the book in the exploration of novel therapeutic opportunities. 2023 PROSE Awards - Winner: Category: Biomedicine and Neuroscience: Association of American Publishers Provides a thorough introduction to Cellular Senescence Covers all major pathologies for which cellular senescence has shown evidence of involvement Focuses on possible therapeutic pathways Edited and authored by worldwide experts
Cell Senescence by Lorenzo Galluzzi,Ilio Vitale,Oliver Kepp,Guido Kroemer Pdf
Cell senescence is the process whereby cells permanently lose the possibility to proliferate without undergoing cell death, and occurs in a plethora of distinct model organisms. In Cell Senescence: Methods and Protocols, expert researchers in the field detail the methods that are now commonly used to study cell senescence, in model organisms encompassing bacteria, fungi, worms, flies, zebrafish, and mammalian cells. These techniques cover the study of all the morphological, biochemical and functional manifestations of senescence at the cellular level and include protocols for population analyses and high-throughput approaches in suitable model organisms. Written in the highly successful Methods in Molecular BiologyTM 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.
Author : Peter D. Adams,John M. Sedivy Publisher : Springer Science & Business Media Page : 274 pages File Size : 42,7 Mb Release : 2010-01-23 Category : Medical ISBN : 9781441910752
Cellular Senescence and Tumor Suppression by Peter D. Adams,John M. Sedivy Pdf
As cells mature they naturally stop dividing and enter a period called senescence. But cellular senescence can also be induced prematurely by certain oncogenes involved in cancer development. Cellular senescence, a growth-arrest program that limits the lifespan of mammalian cells and prevents unlimited cell proliferation, is attracting considerable interest because of its links to tumor suppression.
Cellular Senescence: Causes, Consequences and Therapeutic Opportunities by Elizabeth Lara Ostler,Richard George Faragher,Efstathios Gonos,Pooi-Fong Wong Pdf
Aging of Cells in and Outside the Body by S. Kaul,Renu Wadwha Pdf
This book provides updated knowledge on the basic features and mechanisms of cellular aging established since its first manifestation at cellular level 40 years ago. Contributions of genetic and environmental factors, failure of genetic and cellular repair mechanisms, and the epigenetic modifications determine the final lifespan of cells. This book also provides an understanding on how aging mechanisms in mice, a most frequently used model, differ with that of humans who receive better tumor surveillance because of stringent controls on aging mechanisms. It also appraises the use of modern technology for aging studies and its intervention. This book serves as an excellent reading on cellular aging for undergraduate students, researchers and experts of this area.
The Biology of Senescence by Bernard Swynghedauw Pdf
This book describes the fundamental process of senescence, and reviews a new concept developed by a number of research groups that is based on cellular senescence and its secretome. This concept provides a basic explanation of the main physiological and pathological features of senescence, and delineates possibilities for “treating” it. Following an introduction to the emerging medical landscape, the increasing incidence of a new epidemiological group (age-related “chronic non-transmissible diseases”), and the multiple origins of aging, the book explores and characterizes the senescent cell, which is linked to benign and pathological age-related manifestations. In turn, the closing chapters discuss how to “treat” or “prevent” the aging process, underscoring the central role of physical exercise and caloric reduction as compared to new senolytic approaches. Appendices are also provided, and address circadian rhythms, telomere shortening, diabetic cardiomyopathy, and senescence in plants and bacteria. Given its scope, the book will primarily be of interest to geriatricians, but will also appeal to a wider range of clinicians.
Cellular Aging and Cell Death by Nikki J. Holbrook,George R. Martin,Richard A. Lockshin Pdf
Cellular AGING AND CELL DEATH Edited by Nikki J. Holbrook, George R. Martin, and Richard A.Lockshin Cellular Aging and Cell Death provides a thorough understanding ofthe mechanisms responsible for cellular aging, covering the recentresearch on programmed cell death and senescence, and describingtheir role in the control of cell proliferation and the agingprocess. This one-of-a-kind book is the first to combine the twohottest research areas of cell biology into one comprehensivetext. Leading experts contribute to give readers an authoritativeoverview of the distinct fields of cellular aging and programmedcell death, as well as to demonstrate how both fields are criticalto understanding the aging process. They address the large andgrowing interest in apoptosis, especially with regard to themolecular signals that induce and regulate programmed cell death,and the role of apoptosis in a variety of age-associated diseasesand disabilities. Throughout the book, a strong emphasis is placedon the interrelationship of the molecular, cellular, andphysiological aspects of senescence. Individual chapters discuss such topics as the role and regulationof apoptosis in development, the potential impact of cell death onsuch postmitotic tissues as nerve and muscle, and suggest thatprogrammed cell death plays an important role in both pathologicaland nonpathological aspects of aging, including neurodegenerativediseases. One important chapter focuses on the most recent research involvingthe study of telomeres, whose reduction in length with age and celldivision may underlie cellular senescence. The subject of neuronalcell death is also put into the perspective of aging. Cellular Aging and Cell Death bridges the rapidly growing fields ofcellular aging and programmed cell death. This thorough, yetconcise book will be of particular interest to graduate studentsand researchers within the fields of cell and developmentalbiology, neurobiology, immunology, and physiology. Physicians andmedical students involved in the fields of gerontology andpathology will also find this an informative reference.
This monograph, Senescence; Dominant or Recessive In Somatic Cell Crosses? represents the second annual workshop to promote theory and concept development in aging research. These workshops are part of a resource to bank cultured cells of special interest to aging research that was established at the Institute for Medical Research in Camden. New Jersey. by the National Institute on Aging in 1974. The underlying theme of the workshops is the use of cultured cells in a variety of somatic cell genetic systems designed to define mechanisms of in vitra cellular scen escence and the possible insights that this may provide to the problems of in viva aging. The concept also includes bringing together workers from a variety of disciplines to stimulate new and innovative thoughts and work in the area. The current work shop focuses on the relative role of nucleus and cytoplasm on determining the in vitra lifespan of human diploid cells as well as the relative influence of old and young cells when combined within a single cell structure. The techniques and procedures discussed should make significant contributions to understanding in vitra senescence and may lead to the mapping of an area or areas of the genome linked to senescence as is being accomplished with viral transformation of normal cells. Warren W. Nichols Donald G. Murphy ~i Contents Theoretic Mechanisms of in vitpo Senescence 1 F. MaPott Sinex . . . . . . . . . . . . Senescence in Ce1l Cu1ture: An Accumu1ation of Errors or Terminal Differentiation? 13 Vincent J. GPistofaZo . . . . . . . . . . . . . .
Cellular Senescence and Aging, Volume 181 in the Methods in Cell Biology series, highlights new advances in the field, with this new volume presenting interesting chapters on topics such as assessing polyglutamine tract aggregation in the nematode Caenorhabditis elegans, Generation of glial cell-derived neurotrophic factor (gdnf) morphants in zebrafish larvae by cerebroventricular microinjection of vivo morpholino, Methods for detection of mitochondrial reactive oxygen species in senescent cells, Assessment of cell cycle progression and mitotic slippage by videomicroscopy, The original colorimetric method to detect cellular senescence, and more. Additional sections cover Assessing microbiota composition in the context of aging, Assessing chronological aging in Saccharomyces cerevisiae, Image processing and supervised machine learning for retinal microglia characterization in senescence, Measuring telomerase activity using TRAP assays, High throughput assessment of cellular senescence, Detection of radiation-induced senescence by the Debacq-Chainiaux protocol: Improvements and upgrade in the detection of positive events, Dynamic and scalable assessment of the senescence-associated secretory phenotype (SASP), Flow cytometry-assisted quantification of cell cycle arrest in cancer cells treated with CDK4/6 inhibitors, and more. Provides the authority and expertise of leading contributors from an international board of authors Presents the latest release in the Methods in Cell Biology series Updated release includes the latest information on Cellular Senescence and Aging
Cellular Senescence by Razmik Mirzayans,David Murray (Ph. D.) Pdf
Normal human cells have a limited life span when grown in culture. Aging cells enter a state of permanent growth arrest called replicative senescence, which is regulated by multiple signal transduction pathways involving p53 and other cancer-associated proteins. Senescent cells exhibit flattened and enlarged morphology, retain cell membrane integrity, remain metabolically active, but cease to divide when explanted in culture. Exposure of young (early passage) human cells to genotoxic agents such as ionising radiation and cancer therapeutic drugs can also trigger a state of permanent growth arrest. One mechanism of stress-induced growth arrest is similar to replicative senescence and is commonly termed accelerated or premature senescence. Whereas some normal human cell types (e.g., skin fibroblasts) lose their clonogenic potential in response to genotoxic stress primarily through the process of premature senescence, it has been generally assumed that cancer-derived cells die through necrosis or programmed cell death (apoptosis) but do not exhibit premature senescence following exposure to genotoxic agents. Recently, however, it has become evident that exposure of human solid tumour-derived cells to genotoxic agents can trigger not only premature senescence, but also growth arrest by an ill-defined process leading to the development of multinucleated/polyploid cells. Here the author provides evidence reinforcing the notion that ionising radiation-triggered premature senescence in cancer cells is generally dependent on the wild-type p53 function, and that the development of giant cells is a response of p53-deficient cells, presumably reflecting their failure to engage the premature senescence program.
New Research on Cell Aging by Reginald B. Garvey Pdf
This book presents research on cell growth and the ageing process. Emphasis is given to implications for cancer therapy, abnormal mitosis and aberrant nuclear morphology, neoplastic transformations, negative charges on various malignant cell types.
Cellular Senescence in Health, Disease and Aging: Blessing Or Curse? by Markus Riessland Pdf
Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor.
