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This book is a systematic collection and critical analysis of current information on rejuvenation, starting from the evolutionary aspects of the origin of life, immortality, and aging. Models, mechanisms, and types of rejuvenation are the key subjects of the book. Processes like cellular reprogramming, resetting of the aging clock, immortal unicellulars and cell cultures are explored through the lens of rejuvenation. Recent discoveries in this field offer a nuanced view of rejuvenation that has fascinated mankind since early history. There is evidence, though still controversial, indicating that biological time could be reversible. Indeed, under specific experimental conditions, cells can be moved back and forth along the age axis. Differentiation status and replicative age of cells can be modified not only by defined transcription factors, but also by ‘cocktails’ of small molecules originating from natural substances or well-known longevity-promoting drugs. Still in its infancy, such findings open up the perspective of in vivo rejuvenation trials. Special attention is given to the quasi-immortal and extremely long-lived multicellular animal species as well as to the role of rejuvenation in treatment of pathology and healthy aging. Rejuvenation is experiencing a significant growth in recent years. There is ample debate in the scientific and near-scientific community about the ethics of rejuvenation and radical life span extension. This book aims to take a balanced and scientific approach to the mirage of immortality and ever-lasting youth and serves as a valuable resource for parties on both sides of the coin.

Aging. --- Stem cells. --- Geriatrics. --- Cytology. --- Medicine --- Biology --- Ageing. --- Stem Cell Biology. --- Cellular Senescence. --- Biomedical Research. --- Research.

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This book provides a comprehensive understanding of cellular senescence, which is a phenomenon, characterized by the irreversible arrest of cell growth and is accompanied by the secretion of various factors, collectively known as the senescence-associated secretory phenotype (SASP), which can have detrimental effects on surrounding cells and tissues. The book examines the role of cellular senescence as a driver of age-related disorders such as cancer, neurodegenerative diseases, cardiovascular conditions, and metabolic disorders. By elucidating the molecular mechanisms involved, the book aims to deepen our understanding of these complex diseases and identify potential therapeutic targets. The book also explores cutting-edge therapeutic modalities that target cellular senescence, ranging from small molecule inhibitors to gene-based therapies and regenerative approaches. The distinctive features of the book include its comprehensive approach, integration of multidisciplinary expertise, in-depth exploration of therapeutic modalities, evidence-based insights supported by scientific research, and a translational focus. The interdisciplinary collaboration ensures a holistic understanding of the subject matter, fostering a synergistic approach to addressing age-related disorders. The book not only discusses the potential of emerging therapeutic modalities but also emphasizes practical implications, providing a bridge between research and real-world applications. This book is useful to researchers, scientists, and academics in the fields of molecular biology, genetics, gerontology, and cellular biology.

Medicine --- Biology --- Clinical biochemistry. --- Neuropharmacology. --- Cytology. --- Aging. --- Neurophysiology. --- Neurons. --- Biomedical Research. --- Medical Biochemistry. --- Cellular Senescence. --- Cellular Neuroscience. --- Research.

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Cell death --- Cell Death. --- Cell death. --- Cell degeneration --- Death, Cell --- Cells --- Death (Biology) --- Cellular Senescence --- cell death --- cell biology --- cancer --- neurobiology --- inflammation --- Histology. Cytology --- Oncology. Neoplasms

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General embryology. Developmental biology --- Cell Aging. --- Cell Survival. --- Cells --- Cellules --- Aging. --- Vieillissement --- Aging --- Cell Viability --- Cell Viabilities --- Survival, Cell --- Viabilities, Cell --- Viability, Cell --- Cell Growth Processes --- Aging, Biological --- Biological Aging --- Senescence --- Mutation Accumulation --- Cellular Senescence. --- Cell Survival --- Cells - Aging

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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

Research & information: general --- Biology, life sciences --- γH2AX --- Alzheimer's disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3