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Cell. 2017 Jun 1;169(6):1000-1011. doi: 10.1016/j.cell.2017.05.015.

Senescence in Health and Disease.

Author information

1
Departments of Medicine and Genetics, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7295, USA; The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7295, USA.
2
Departments of Medicine and Genetics, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7295, USA; The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7295, USA. Electronic address: nes@med.unc.edu.

Abstract

Many cellular stresses activate senescence, a persistent hyporeplicative state characterized in part by expression of the p16INK4a cell-cycle inhibitor. Senescent cell production occurs throughout life and plays beneficial roles in a variety of physiological and pathological processes including embryogenesis, wound healing, host immunity, and tumor suppression. Meanwhile, the steady accumulation of senescent cells with age also has adverse consequences. These non-proliferating cells occupy key cellular niches and elaborate pro-inflammatory cytokines, contributing to aging-related diseases and morbidity. This model suggests that the abundance of senescent cells in vivo predicts "molecular," as opposed to chronologic, age and that senescent cell clearance may mitigate aging-associated pathology.

KEYWORDS:

DNA damage; SASP; aging; cancer; cellular senescence; molecular age; p16(INK4a); senolysis; telomere; tumor suppression

PMID:
28575665
PMCID:
PMC5643029
DOI:
10.1016/j.cell.2017.05.015
[Indexed for MEDLINE]
Free PMC Article

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