Cellular Senescence in Disease

Cellular Senescence in Disease

1st Edition - November 27, 2021

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  • Editors: Manuel Serrano, Daniel Munoz-Espin
  • eBook ISBN: 9780128225158
  • Paperback ISBN: 9780128225141

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Description

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.

Key Features

  • 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

Readership

Researchers and clinicians with a focus on the cellular mechanisms of diseases

Table of Contents

  • Cover image
  • Title page
  • Table of Contents
  • Copyright
  • Contributors
  • Foreword
  • Part 1. Fundamentals
  • Chapter 1. Cellular senescence: from old to new testament
  • Old testament—genesis of senescence
  • New testament—from mechanisms and roles of senescence to therapies
  • Part 2. Cellular senescence in disease states
  • Chapter 2. Premalignant lesions and cellular senescence
  • Introduction
  • Cellular senescence in premalignant lesions: evidence in various organs
  • Future perspectives
  • Chapter 3. Lung aging and senescence in health and disease
  • Introduction
  • Normal lung development and aging
  • A brief introduction to COPD and IPF
  • Abnormal hallmarks of lung aging in COPD and IPF
  • Future treatment targeting lung senescence
  • Conclusions
  • Supported
  • Abbreviations
  • Chapter 4. Cell senescence in pulmonary hypertension
  • Introduction
  • Pulmonary hypertension, a non-aging-related proliferative vascular disorder at the crossroads of vascular disease and cancer
  • General considerations about aging of the systemic and pulmonary vascular systems
  • Considerations about constitutive cells of pulmonary vessels and the specificity of the pulmonary vasculature
  • Potential mechanisms accounting for cell senescence in PH and PAH
  • Role for senescent cells in PH and PAH
  • Conclusion
  • Chapter 5. Liver diseases fibrosis and cirrhosis
  • Liver structure and function
  • Cellular senescence
  • Liver diseases—epidemiology and clinical aspects
  • Senescence during aging of the healthy liver
  • Senescence in acute liver injury
  • Senescence in chronic liver disease
  • Role of senescence in hepatic dysfunction
  • Evolutionary role of senescence in the liver
  • Senescence during hepatic carcinogenesis
  • Summary and closing comments
  • Chapter 6. Cellular senescence during aging and chronic liver diseases: mechanisms and therapeutic opportunities
  • Introduction
  • Cellular senescence in the liver
  • Mechanisms contributing to cellular senescence in liver
  • Therapies: senolytic and senostatic drugs
  • Conclusions and outstanding questions
  • List of abbreviations
  • Chapter 7. Kidney diseases: fibrosis
  • Introduction
  • Fibrosis is a common feature of unresolved kidney damage and kidney aging
  • Glomerulosclerosis, vascular sclerosis, tubulointerstitial fibrosis
  • ECM in renal homeostasis, injury, and repair
  • Cellular senescence in renal aging, AKI, and CKD
  • Different forms and different timing of cell-cycle arrest may have detrimental or beneficial effects in AKI and CKD
  • TIF and cellular senescence
  • Senescence and the cellular origin of TIF
  • Senescence-associated secretory phenotype
  • Transforming growth factor-β (TGF-β)
  • WNT/β-catenin signaling
  • The renin-angiotensin system (RAS)
  • The antiaging factor Klotho
  • Inflammation, innate immunity, and TIF
  • Senescence and TIF—physiology and pathology
  • Chapter 8. Kidney diseases: transplantation
  • Introduction
  • Factors determining donor organ quality and their association with senescence
  • Impact of cellular senescence on transplant-related injuries and transplant outcome
  • Rejuvenating and protecting kidney transplants
  • Chapter 9. Vascular diseases: atherosclerosis and atherosclerotic cardiovascular diseases
  • Introduction—“a man is as old as his arteries”
  • Features of cellular senescence in vascular cells
  • Evidence of cellular senescence in atherosclerosis
  • Factors involved in vascular senescence associated with the pathophysiology of atherosclerosis
  • Therapeutics targeting cellular senescence for atherosclerosis
  • Conclusions (limitations and perspectives)
  • Chapter 10. Diabetes: senescence in type 1 diabetes
  • Introduction
  • Senescent beta cell accumulation as a novel pathogenic mechanism in T1D
  • Outstanding questions and future directions
  • Conclusions and outlook
  • Chapter 11. Senescence in obesity: causes and consequences
  • Introduction
  • Adipose tissue function in obesity
  • Senescent cells accumulate in multiple tissues in obesity
  • Causes of cellular senescence in obesity
  • Threshold theory of senescent cell burden
  • Implications of senescence in obesity: downstream effects
  • Strategies to target obesity-related senescent cells
  • Chapter 12. A framework for addressing senescent cell burden in the osteoarthritic knee: therapeutics, immune signaling, and the local-systemic interface
  • Introduction
  • Main
  • Conclusion
  • Competing interests
  • Chapter 13. Osteoporosis and bone loss
  • Osteoporosis as a public health problem
  • The hallmarks of aging in bone
  • The role of cellular senescence in mediating age-related bone loss
  • Estrogen deficiency and cellular senescence
  • The role of cellular senescence in the effects of diabetes mellitus on bone
  • Cellular senescence and radiation- and chemotherapy-induced bone loss
  • Role of cellular senescence in the growth plate and regulation by parathyroid hormone–related peptide (PTHrP)
  • Summary and conclusions
  • Chapter 14. Cellular senescence in neurodegenerative diseases
  • Cellular senescence: driving force or beneficial response in neurodegeneration?
  • Postmitotic senescence in brain aging and neurodegenerative diseases
  • Replicative senescence in brain aging and neurodegenerative diseases
  • Demyelination, oligodendrocyte lineages, and Aβ plaque propagation in AD brains
  • Senolytics as AD therapy
  • Combination therapy for AD using senolytics and senomorphics
  • Conclusions
  • Chapter 15. Cell senescence is a cause of frailty
  • What is frailty?
  • How is frailty assessed in humans?
  • How is frailty defined and assessed in experimental animals?
  • What are the possible causes of frailty?
  • What is cell senescence?
  • Does cell senescence cause frailty? How good is the evidence for it?
  • Conclusions
  • Part 3. Conclusions
  • Chapter 16. Senescence as a therapeutic target: current state and future challenges
  • Biological interpretations of cellular senescence
  • Tissue remodeling by senescence is a two-step process
  • The two steps of senescence in cancer
  • The two steps of senescence in disease
  • SASP-induced tissue repair versus SASP-induced tissue dysfunction
  • Molecular triggers of senescence
  • Triggers of senescence in vivo
  • The challenge of detecting cellular senescence in clinical settings
  • Potential side effects of eliminating senescent cells
  • Senolytics as an anti-aging strategy
  • Index

Product details

  • No. of pages: 472
  • Language: English
  • Copyright: © Academic Press 2021
  • Published: November 27, 2021
  • Imprint: Academic Press
  • eBook ISBN: 9780128225158
  • Paperback ISBN: 9780128225141

About the Editors

Manuel Serrano

Dr. Manuel Serrano did his PhD under the supervision of Margarita Salas (CBM-CSIC, Madrid) and a postdoctoral stay in David Beach’s lab (Cold Spring Harbor Laboratory, NY, USA) from 1992 to 1996. During this time, he made one of his most important contributions, namely the discovery of the tumor suppressor p16. The main contributions of Dr. Serrano’s lab during these years are related to the concept of oncogene-induced senescence and the anti-ageing activity of tumor suppressors. More recently, his group has reported on the relevance of tumor suppressors in metabolic syndrome, the existence of senescence during embryonic development, and the feasibility of embryonic reprogramming within living adult organisms (the latter was considered "Achievement of the Year 2013" in the stem cells field by Nature Medicine).

Affiliations and Expertise

Parc Científic de Barcelona, Baldiri Reixa, Barcelona, Spain

Daniel Munoz-Espin

Dr. Daniel Munoz-Espin is Senior Research Associate at the Department of Oncology of the University of Cambridge. His lab is part of the CRUK Cambridge Centre Early Detection Programme, working at interface between cellular senescence, plasticity and the fundamental processes and mechanisms that lie at the origin of cancer. We are also developing novel tools and nanodevices for cancer therapy and diagnosis.

Affiliations and Expertise

Senior Research Associate, Department of Oncology, University of Cambridge, Cambridge, UK

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