Cellular senescence and the senescent secretory phenotype: therapeutic opportunities

Aging is the largest risk factor for most chronic diseases, which account for the majority of morbidity and health care expenditures in developed nations. New findings suggest that aging is a modifiable risk factor, and it may be feasible to delay age-related diseases as a group by modulating fundam...

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Bibliographic Details
Published in:The Journal of clinical investigation 2013-03, Vol.123 (3), p.966-966
Main Authors: Tchkonia, Tamara, Zhu, Yi, van Deursen, Jan, Campisi, Judith, Kirkland, James L
Format: Article
Language:English
Subjects:
Age
Aging
Aging - drug effects
Aging - immunology
Aging - pathology
Animals
Apoptosis
Atherosclerosis
Biomedical research
Cancer
Cardiovascular disease
Cell division
Cellular Senescence - drug effects
Cellular Senescence - immunology
Chemokines
Chronic illnesses
Clinical Trials as Topic
Cytokines
Dementia
Diabetes
Disability
DNA Damage
DNA Repair
Frailty
Genotype & phenotype
Humans
Immune system
Inflammation
Inflammation Mediators - metabolism
Inflammation Mediators - physiology
Molecular Targeted Therapy
Mortality
Older people
Phenotype
Proteins
Review Series
Risk factors
Senescence
Signal Transduction
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Summary:Aging is the largest risk factor for most chronic diseases, which account for the majority of morbidity and health care expenditures in developed nations. New findings suggest that aging is a modifiable risk factor, and it may be feasible to delay age-related diseases as a group by modulating fundamental aging mechanisms. One such mechanism is cellular senescence, which can cause chronic inflammation through the senescence-associated secretory phenotype (SASP). We review the mechanisms that induce senescence and the SASP, their associations with chronic disease and frailty, therapeutic opportunities based on targeting senescent cells and the SASP, and potential paths to developing clinical interventions.
ISSN:0021-9738
1558-8238
DOI:10.1172/JCI64098