| Senescence and life span. | |
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MedLine Citation:
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PMID: 19763609 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Senescence is a general cellular process that occurs as a response to stress and damage. It forms an alternative response of cells to damage that might otherwise cause programmed cell death. Whereas telomere shortening leading to telomere dysfunction was the first described cause of senescence, it is now known that senescence can result from many sources of damage. Senescent cells are found in tissues in vivo, but the cause of senescence in these cells is mostly unknown. In many cases, senescence may be the result of the action of activated oncogenes in cells. By preventing activated oncogenes from initiating a clone of neoplastic cells, senescence acts as a protective mechanism against cancer development. Until recently, the fate of senescent cells in vivo was unknown, but new evidence indicates that they are cleared by components of the innate immune system. In this way, senescence and apoptosis act as parallel pathways by which severely damaged cells are eliminated from the body. Some senescent cells persist in tissues, in some cases increasing in frequency as a function of age. It is hypothesized that these persistent senescent cells have adverse effects on tissue function. If so, senescence may be an example of antagonistic pleiotropy, providing an anticancer mechanism in early life but having adverse effects on tissue function in late life. Much more research is needed to address the broader question of the overall impact of senescence on life span. |
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Authors:
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Peter J Hornsby |
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Publication Detail:
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Type: Journal Article; Review Date: 2009-09-08 |
Journal Detail:
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Title: Pfl?gers Archiv : European journal of physiology Volume: 459 ISSN: 1432-2013 ISO Abbreviation: Pflugers Arch. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-01-21 Completed Date: 2010-03-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0154720 Medline TA: Pflugers Arch Country: Germany |
Other Details:
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Languages: eng Pagination: 291-9 Citation Subset: IM |
Affiliation:
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Department of Physiology and Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, Texas, USA. hornsby@uthscsa.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aging
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genetics* Animals Cell Aging / genetics* DNA Damage / physiology Heterochromatin / physiology Humans Inflammation / physiopathology Longevity / genetics Lysosomes / enzymology Neoplasms / genetics Oncogenes / physiology Signal Transduction / physiology Telomere / physiology beta-Galactosidase / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Heterochromatin; EC 3.2.1.23/beta-Galactosidase |
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