title: The senescence arrest program and the cell cycle.
abstract: All living organisms are subject to progressive loss of function and damage to their tissues, a process known as aging. At the cellular level, the accumulation of damage to DNA, proteins, and organelles induces cellular senescence, a stress-response pathway that likely influences the aging process. Although the senescence arrest program was initially described in vitro, accumulating evidence suggests that this damage response program occurs in a variety of pathologic settings. This review discusses aspects of the senescence program, their interrelationships with damage arrest pathways, the cell cycle, and the impact of senescence in vivo.
authors.affiliation: Department of Pathology, University of Washington, Health Science Building D-514, Seattle, 357470, WA, USA.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Bitto
authors.forename: Elizabeth P
authors.initials: EP
authors.lastname: Crowe
authors.forename: Chad
authors.initials: C
authors.lastname: Lerner
authors.forename: Claudio
authors.initials: C
authors.lastname: Torres
authors.forename: Christian
authors.initials: C
authors.lastname: Sell
mesh_terms: D000818:Animals; D002453:Cell Cycle; D016922:Cellular Senescence; D002843:Chromatin / Q000235:genetics / Q000378:metabolism; D004247:DNA / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D002843:Chromatin; D017382:Reactive Oxygen Species; D004247:DNA