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Cellular senescence in disease /
| Clasificación: | Libro Electrónico |
|---|---|
| Otros Autores: | , |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
London :
Academic Press,
2022.
|
| Temas: | |
| Acceso en línea: | Texto completo |
Tabla de Contenidos:
- Front Cover
- Cellular Senescence in Disease
- Cellular Senescence in Disease
- Copyright
- Contents
- Contributors
- Foreword
- REFERENCES
- 1
- Fundamentals
- 1
- Cellular senescence: from old to new testament
- Old testament-genesis of senescence
- New testament-from mechanisms and roles of senescence to therapies
- Replicative senescence and telomeres
- Oncogene-induced senescence and tumor suppression
- Damage-induced senescence
- Hallmarks of cellular senescence
- SASP
- Senescence in physiology, repair, and embryonic development
- Senescence in aging and age-related disorders
- Prosenescent and antisenescent therapies
- Clinical trials
- References
- 2
- Cellular senescence in disease states
- 2
- Premalignant lesions and cellular senescence
- Introduction
- Cellular senescence in premalignant lesions: evidence in various organs
- Skin
- Head and neck
- Lungs
- Gastrointestinal tract
- Liver
- Pancreas
- Mammary gland
- Prostate gland
- Cervix
- Thyroid
- Future perspectives
- References
- Further reading
- 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
- Cellular senescence
- Mitochondrial dysfunction
- Stem cell dysfunction
- Telomere dysfunction
- Epigenetic changes and miRNAs
- Loss of protein homeostasis (proteostasis)
- Deregulated nutrient sensing
- Extracellular matrix (ECM) dysregulation
- Future treatment targeting lung senescence
- Conclusions
- Supported
- Abbreviations
- References
- 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
- DNA damage is associated with PH
- Pulmonary artery smooth muscle cells (PASMCs)
- Pulmonary vascular endothelial cells (PECs)
- Genetic and environmental factors responsible for DNA damage in PAH
- The link between DNA damage, cell senescence, and PAH pathogenesis
- Alteration in the BMPR2/TGF beta pathway
- Hypoxia
- Drugs
- Telomere dysfunction
- Shear stress
- HIV infection
- Role for senescent cells in PH and PAH
- General considerations
- Induction of lung cell senescence: effect on PH
- Treatment with nutlin
- Telomerase inactivation
- Induction of cell senescence by activation of signaling pathways involved in chronic lung diseases
- Prevention or protection against lung cell senescence: effect on PH
- Inactivation of p53, p21, p16
- Elimination of senescent cells in experimental PAH
- Conclusion
- References
- 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
- References
- 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
- Telomere dysfunction
- Autophagy impairment
- Mitochondrial dysfunction.
- Fatty acids
- Oxidative stress
- Telomere shortening
- Growth hormone axis
- mTOR activity
- Altered microbiome
- Threshold theory of senescent cell burden
- Implications of senescence in obesity: downstream effects
- Inflammation
- Inhibition of adipogenesis and ectopic lipid deposition
- NAD+ depletion due to CD38+ macrophage attraction
- Obesity-induced neurocognitive defects
- Paracrine effects on neighboring cells
- Promotion of cancer development
- Reduced regenerative potential
- Strategies to target obesity-related senescent cells
- Exercise and weight loss
- Senolytics
- SASP inhibitors or senomorphics
- Administration schedule of senescence-targeting therapies
- References
- 12
- A framework for addressing senescent cell burden in the osteoarthritic knee: therapeutics, immune signaling, a ...
- Introduction
- Main
- Knee tissues degenerate in osteoarthritis
- Chronic presence of senescent cells in the knee accelerates osteoarthritic erosion
- Killing senescent cells in the knee can reduce OA-associated dysfunction
- Translating antisenescent therapies to the clinic for OA treatment
- Conclusion
- Competing interests
- References
- 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
- Identification of senescent cells in the bone microenvironment
- Causal role for cellular senescence in mediating age-related bone loss
- Role of cellular senescence in mediating age-related frailty
- 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.