Molecular bases of cellular senescence: Hayflick phenomenon 50 years later
Normal human somatic cells have strictly limited proliferative capacity and reach a state of senescence when it becomes exhausted. It is believed that senescence is a response to extensive and irreparable DNA injury, localized in telomeric and/or non-telomeric regions of the genome. Main cause of th...
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doaj-132de4236b2f465d8a7adb515436dcb52020-11-25T01:55:09ZengIndex Copernicus International S.A.Postępy Higieny i Medycyny Doświadczalnej0032-54491732-26932016-03-017023124210.5604/01.3001.0009.680301.3001.0009.6803Molecular bases of cellular senescence: Hayflick phenomenon 50 years laterPatrycja Sosińska0Justyna Mikuła-Pietrasik1Krzysztof Książek2Katedra i Zakład Patofizjologii, Uniwersytet Medyczny im. Karola Marcinkowskiego w PoznaniuKatedra i Zakład Patofizjologii, Uniwersytet Medyczny im. Karola Marcinkowskiego w PoznaniuKatedra i Zakład Patofizjologii, Uniwersytet Medyczny im. Karola Marcinkowskiego w PoznaniuNormal human somatic cells have strictly limited proliferative capacity and reach a state of senescence when it becomes exhausted. It is believed that senescence is a response to extensive and irreparable DNA injury, localized in telomeric and/or non-telomeric regions of the genome. Main cause of this damage is oxidative stress, increasing due to deteriorated function of mitochondria. Senescent cells accumulate in tissues during aging, which is causatively linked with the development of various pathologies in elderly individuals, including cancer. This paper, prepared exactly 50 years after Leonard Hayflick’s discovery of the relationship between cellular senescence and organismal aging is aimed at presenting the current knowledge about molecular determinants of senescence, with particular emphasis paid to the role of oxidative stress, effectors of senescence at the level of cell cycle, markers of this phenomenon, and the effect of senescent cells on the development of certain age-related diseases. http://phmd.pl/gicid/01.3001.0009.6803onkogenezastarzenie komórkowetelomeryuszkodzenia DNAcellular senescenceDNA Damage |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Patrycja Sosińska Justyna Mikuła-Pietrasik Krzysztof Książek |
spellingShingle |
Patrycja Sosińska Justyna Mikuła-Pietrasik Krzysztof Książek Molecular bases of cellular senescence: Hayflick phenomenon 50 years later Postępy Higieny i Medycyny Doświadczalnej onkogeneza starzenie komórkowe telomery uszkodzenia DNA cellular senescence DNA Damage |
author_facet |
Patrycja Sosińska Justyna Mikuła-Pietrasik Krzysztof Książek |
author_sort |
Patrycja Sosińska |
title |
Molecular bases of cellular senescence: Hayflick phenomenon 50 years later |
title_short |
Molecular bases of cellular senescence: Hayflick phenomenon 50 years later |
title_full |
Molecular bases of cellular senescence: Hayflick phenomenon 50 years later |
title_fullStr |
Molecular bases of cellular senescence: Hayflick phenomenon 50 years later |
title_full_unstemmed |
Molecular bases of cellular senescence: Hayflick phenomenon 50 years later |
title_sort |
molecular bases of cellular senescence: hayflick phenomenon 50 years later |
publisher |
Index Copernicus International S.A. |
series |
Postępy Higieny i Medycyny Doświadczalnej |
issn |
0032-5449 1732-2693 |
publishDate |
2016-03-01 |
description |
Normal human somatic cells have strictly limited proliferative capacity and reach a state of senescence when it becomes exhausted. It is believed that senescence is a response to extensive and irreparable DNA injury, localized in telomeric and/or non-telomeric regions of the genome. Main cause of this damage is oxidative stress, increasing due to deteriorated function of mitochondria. Senescent cells accumulate in tissues during aging, which is causatively linked with the development of various pathologies in elderly individuals, including cancer. This paper, prepared exactly 50 years after Leonard Hayflick’s discovery of the relationship between cellular senescence and organismal aging is aimed at presenting the current knowledge about molecular determinants of senescence, with particular emphasis paid to the role of oxidative stress, effectors of senescence at the level of cell cycle, markers of this phenomenon, and the effect of senescent cells on the development of certain age-related diseases.
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topic |
onkogeneza starzenie komórkowe telomery uszkodzenia DNA cellular senescence DNA Damage |
url |
http://phmd.pl/gicid/01.3001.0009.6803 |
work_keys_str_mv |
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