The signals and pathways activating cellular senescence
Cellular senescence is a program activated by normal cells in response to various types of stress. These include telomere uncapping, DNA damage, oxidative stress, oncogene activity and others. Senescence can occur following a period of cellular proliferation or in a rapid manner in response to acute...
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Veröffentlicht in: | The international journal of biochemistry & cell biology 2005-05, Vol.37 (5), p.961-976 |
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description | Cellular senescence is a program activated by normal cells in response to various types of stress. These include telomere uncapping, DNA damage, oxidative stress, oncogene activity and others. Senescence can occur following a period of cellular proliferation or in a rapid manner in response to acute stress. Once cells have entered senescence, they cease to divide and undergo a series of dramatic morphologic and metabolic changes. Cellular senescence is thought to play an important role in tumor suppression and to contribute to organismal aging, but a detailed description of its physiologic occurrence in vivo is lacking. Recent studies have provided important insights regarding the manner by which different stresses and stimuli activate the signaling pathways leading to senescence. These studies reveal that a population of growing cells may suffer from a combination of different physiologic stresses acting simultaneously. The signaling pathways activated by these stresses are funneled to the p53 and Rb proteins, whose combined levels of activity determine whether cells enter senescence. Here we review recent advances in our understanding of the stimuli that trigger senescence, the molecular pathways activated by these stimuli, and the manner by which these signals determine the entry of a population of cells into senescence. |
doi_str_mv | 10.1016/j.biocel.2004.10.013 |
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These include telomere uncapping, DNA damage, oxidative stress, oncogene activity and others. Senescence can occur following a period of cellular proliferation or in a rapid manner in response to acute stress. Once cells have entered senescence, they cease to divide and undergo a series of dramatic morphologic and metabolic changes. Cellular senescence is thought to play an important role in tumor suppression and to contribute to organismal aging, but a detailed description of its physiologic occurrence in vivo is lacking. Recent studies have provided important insights regarding the manner by which different stresses and stimuli activate the signaling pathways leading to senescence. These studies reveal that a population of growing cells may suffer from a combination of different physiologic stresses acting simultaneously. The signaling pathways activated by these stresses are funneled to the p53 and Rb proteins, whose combined levels of activity determine whether cells enter senescence. 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These include telomere uncapping, DNA damage, oxidative stress, oncogene activity and others. Senescence can occur following a period of cellular proliferation or in a rapid manner in response to acute stress. Once cells have entered senescence, they cease to divide and undergo a series of dramatic morphologic and metabolic changes. Cellular senescence is thought to play an important role in tumor suppression and to contribute to organismal aging, but a detailed description of its physiologic occurrence in vivo is lacking. Recent studies have provided important insights regarding the manner by which different stresses and stimuli activate the signaling pathways leading to senescence. These studies reveal that a population of growing cells may suffer from a combination of different physiologic stresses acting simultaneously. The signaling pathways activated by these stresses are funneled to the p53 and Rb proteins, whose combined levels of activity determine whether cells enter senescence. Here we review recent advances in our understanding of the stimuli that trigger senescence, the molecular pathways activated by these stimuli, and the manner by which these signals determine the entry of a population of cells into senescence.</description><subject>ARF</subject><subject>Cellular Senescence</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - physiology</subject><subject>DNA Damage</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Oncogenes - physiology</subject><subject>Oxidative Stress</subject><subject>p16</subject><subject>p53</subject><subject>Retinoblastoma Protein - physiology</subject><subject>Senescence</subject><subject>Signal Transduction</subject><subject>Telomere - chemistry</subject><subject>Telomere - physiology</subject><subject>Telomeres</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><issn>1357-2725</issn><issn>1878-5875</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kFtLwzAYhoMobk7_gUivvGtN0ubQG0HGPMDAm3kd0uTbltG1M2kn-_emdOCdV9-B9_0OD0L3BGcEE_60yyrXGqgzinERWxkm-QWaEilkyqRglzHPmUipoGyCbkLYYYwJo_k1mhAmipwLMkVitYUkuE2j65DoxiYH3W1_9CkWpnNH3blmk8QtdV9rnwRoIBhoDNyiq3W0wN05ztDX62I1f0-Xn28f85dlagrKu7QildRGGMtILkRFLJZcSmatFJprAxRKTGhZcMq4hpKVICgITkBXFutS5jP0OM49-Pa7h9CpvQvDPbqBtg-Ki0JwRkkUFqPQ-DYED2t18G6v_UkRrAZgaqdGYGoANnQjsGh7OM_vqz3YP9OZUBQ8jwKIXx4deBWMGwhY58F0yrbu_w2_ukl9mA</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>Ben-Porath, Ittai</creator><creator>Weinberg, Robert A.</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20050501</creationdate><title>The signals and pathways activating cellular senescence</title><author>Ben-Porath, Ittai ; Weinberg, Robert A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-b1b8ac7cd51377b1d086885dd87a6ace2e9012946256ae959e72e761eabd0a983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>ARF</topic><topic>Cellular Senescence</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - physiology</topic><topic>DNA Damage</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Oncogenes - physiology</topic><topic>Oxidative Stress</topic><topic>p16</topic><topic>p53</topic><topic>Retinoblastoma Protein - physiology</topic><topic>Senescence</topic><topic>Signal Transduction</topic><topic>Telomere - chemistry</topic><topic>Telomere - physiology</topic><topic>Telomeres</topic><topic>Tumor Suppressor Protein p53 - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ben-Porath, Ittai</creatorcontrib><creatorcontrib>Weinberg, Robert A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The international journal of biochemistry & cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ben-Porath, Ittai</au><au>Weinberg, Robert A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The signals and pathways activating cellular senescence</atitle><jtitle>The international journal of biochemistry & cell biology</jtitle><addtitle>Int J Biochem Cell Biol</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>37</volume><issue>5</issue><spage>961</spage><epage>976</epage><pages>961-976</pages><issn>1357-2725</issn><eissn>1878-5875</eissn><abstract>Cellular senescence is a program activated by normal cells in response to various types of stress. 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subjects | ARF Cellular Senescence Cyclin-Dependent Kinase Inhibitor p16 - physiology DNA Damage Gene Expression Regulation Humans Oncogenes - physiology Oxidative Stress p16 p53 Retinoblastoma Protein - physiology Senescence Signal Transduction Telomere - chemistry Telomere - physiology Telomeres Tumor Suppressor Protein p53 - physiology |
title | The signals and pathways activating cellular senescence |
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