Cell Senescence: A Nonnegligible Cell State under Survival Stress in Pathology of Intervertebral Disc Degeneration
The intervertebral disc degeneration (IDD) with increasing aging mainly manifests as low back pain (LBP) accompanied with a loss of physical ability. These pathological processes can be preliminarily interpreted as a series of changes at cellular level. In addition to cell death, disc cells enter in...
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creator | Huang, Xianpeng Yu, Chao Li, Fangcai Liang, Chengzhen Chen, Qixin Xia, Kaishun Wang, Chenggui Ying, Liwei Shi, Kesi Cheng, Feng Wang, Jingkai Yang, Biao Zhang, Yuang Gong, Zhe |
description | The intervertebral disc degeneration (IDD) with increasing aging mainly manifests as low back pain (LBP) accompanied with a loss of physical ability. These pathological processes can be preliminarily interpreted as a series of changes at cellular level. In addition to cell death, disc cells enter into the stagnation with dysfunction and deteriorate tissue microenvironment in degenerative discs, which is recognized as cell senescence. During aging, many intrinsic and extrinsic factors have been proved to have strong connections with these cellular senescence phenomena. Growing evidences of these connections require us to gather up critical cues from potential risk factors to pathogenesis and relative interventions for retarding cell senescence and attenuating degenerative changes. In this paper, we try to clarify another important cell state apart from cell death in IDD and discuss senescence-associated changes in cells and extracellular microenvironment. Then, we emphasize the role of oxidative stress and epigenomic perturbations in linking risk factors to cell senescence in the onset of IDD. Further, we summarize the current interventions targeting senescent cells that may exert the benefits of antidegeneration in IDD. |
doi_str_mv | 10.1155/2020/9503562 |
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These pathological processes can be preliminarily interpreted as a series of changes at cellular level. In addition to cell death, disc cells enter into the stagnation with dysfunction and deteriorate tissue microenvironment in degenerative discs, which is recognized as cell senescence. During aging, many intrinsic and extrinsic factors have been proved to have strong connections with these cellular senescence phenomena. Growing evidences of these connections require us to gather up critical cues from potential risk factors to pathogenesis and relative interventions for retarding cell senescence and attenuating degenerative changes. In this paper, we try to clarify another important cell state apart from cell death in IDD and discuss senescence-associated changes in cells and extracellular microenvironment. Then, we emphasize the role of oxidative stress and epigenomic perturbations in linking risk factors to cell senescence in the onset of IDD. Further, we summarize the current interventions targeting senescent cells that may exert the benefits of antidegeneration in IDD.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/9503562</identifier><identifier>PMID: 32934764</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Aging ; Apoptosis ; Back pain ; Biomarkers ; Cell cycle ; Cell division ; Cell Survival - genetics ; Cellular Microenvironment - genetics ; Cellular Senescence - genetics ; Chronic illnesses ; Deoxyribonucleic acid ; DNA ; DNA damage ; Epigenesis, Genetic ; Epigenetics ; Gene expression ; Growth factors ; Humans ; Intervertebral Disc Degeneration - genetics ; Intervertebral Disc Degeneration - pathology ; Intervertebral Disc Degeneration - therapy ; Kinases ; Oxidative Stress - genetics ; Review ; Senescence</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-12</ispartof><rights>Copyright © 2020 Yuang Zhang et al.</rights><rights>Copyright © 2020 Yuang Zhang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Yuang Zhang et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-c2faccda0922a35dd9c5f35044a9e7938ebec1673376be865d39cec3a2d202a43</citedby><cites>FETCH-LOGICAL-c471t-c2faccda0922a35dd9c5f35044a9e7938ebec1673376be865d39cec3a2d202a43</cites><orcidid>0000-0002-2626-0201 ; 0000-0002-4983-6461 ; 0000-0002-2402-781X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7479476/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7479476/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32934764$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ding, Wenyuan</contributor><contributor>Wenyuan Ding</contributor><creatorcontrib>Huang, Xianpeng</creatorcontrib><creatorcontrib>Yu, Chao</creatorcontrib><creatorcontrib>Li, Fangcai</creatorcontrib><creatorcontrib>Liang, Chengzhen</creatorcontrib><creatorcontrib>Chen, Qixin</creatorcontrib><creatorcontrib>Xia, Kaishun</creatorcontrib><creatorcontrib>Wang, Chenggui</creatorcontrib><creatorcontrib>Ying, Liwei</creatorcontrib><creatorcontrib>Shi, Kesi</creatorcontrib><creatorcontrib>Cheng, Feng</creatorcontrib><creatorcontrib>Wang, Jingkai</creatorcontrib><creatorcontrib>Yang, Biao</creatorcontrib><creatorcontrib>Zhang, Yuang</creatorcontrib><creatorcontrib>Gong, Zhe</creatorcontrib><title>Cell Senescence: A Nonnegligible Cell State under Survival Stress in Pathology of Intervertebral Disc Degeneration</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>The intervertebral disc degeneration (IDD) with increasing aging mainly manifests as low back pain (LBP) accompanied with a loss of physical ability. These pathological processes can be preliminarily interpreted as a series of changes at cellular level. In addition to cell death, disc cells enter into the stagnation with dysfunction and deteriorate tissue microenvironment in degenerative discs, which is recognized as cell senescence. During aging, many intrinsic and extrinsic factors have been proved to have strong connections with these cellular senescence phenomena. Growing evidences of these connections require us to gather up critical cues from potential risk factors to pathogenesis and relative interventions for retarding cell senescence and attenuating degenerative changes. In this paper, we try to clarify another important cell state apart from cell death in IDD and discuss senescence-associated changes in cells and extracellular microenvironment. Then, we emphasize the role of oxidative stress and epigenomic perturbations in linking risk factors to cell senescence in the onset of IDD. Further, we summarize the current interventions targeting senescent cells that may exert the benefits of antidegeneration in IDD.</description><subject>Aging</subject><subject>Apoptosis</subject><subject>Back pain</subject><subject>Biomarkers</subject><subject>Cell cycle</subject><subject>Cell division</subject><subject>Cell Survival - genetics</subject><subject>Cellular Microenvironment - genetics</subject><subject>Cellular Senescence - genetics</subject><subject>Chronic illnesses</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Intervertebral Disc Degeneration - genetics</subject><subject>Intervertebral Disc Degeneration - pathology</subject><subject>Intervertebral Disc Degeneration - therapy</subject><subject>Kinases</subject><subject>Oxidative Stress - genetics</subject><subject>Review</subject><subject>Senescence</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkc1rVDEUxUOp2Fq7cy2BbgSdNt-vcSGUqR-FokLrOuTl3fcm5U1Sk7yR_vdmmHGsrrpKyP1xcs85CL2i5JRSKc8YYeRMS8KlYnvokGrBZkRrsb-7E3KAXuR8R4jiTNDn6IAzzUWjxCFKcxhHfAMBsoPg4D2-wF9jCDCMfvDtCHgDFFsAT6GDhG-mtPIru35MkDP2AX-3ZRHHODzg2OOrUCCtIBVoU6UufXb4Eob6RbLFx_ASPevtmOF4ex6hH58-3s6_zK6_fb6aX1zPnGhomTnWW-c6SzRjlsuu0072XBIhrIZG83NowVHVcN6oFs6V7Lh24LhlXY3ECn6EPmx076d2CV21V-o-5j75pU0PJlpv_p0EvzBDXJlGNLqmUwXebAVS_DlBLmZZvdQ4bIA4ZcOE4JJqLZuKnvyH3sUphWpvTTGqmKSyUu82lEsx5wT9bhlKzLpMsy7TbMus-OvHBnbwn_Yq8HYDLHzo7C__RDmoDPT2L82IIkry37AAsiQ</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Huang, Xianpeng</creator><creator>Yu, Chao</creator><creator>Li, Fangcai</creator><creator>Liang, Chengzhen</creator><creator>Chen, Qixin</creator><creator>Xia, Kaishun</creator><creator>Wang, Chenggui</creator><creator>Ying, Liwei</creator><creator>Shi, Kesi</creator><creator>Cheng, Feng</creator><creator>Wang, Jingkai</creator><creator>Yang, Biao</creator><creator>Zhang, Yuang</creator><creator>Gong, Zhe</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2626-0201</orcidid><orcidid>https://orcid.org/0000-0002-4983-6461</orcidid><orcidid>https://orcid.org/0000-0002-2402-781X</orcidid></search><sort><creationdate>2020</creationdate><title>Cell Senescence: A Nonnegligible Cell State under Survival Stress in Pathology of Intervertebral Disc Degeneration</title><author>Huang, Xianpeng ; Yu, Chao ; Li, Fangcai ; Liang, Chengzhen ; Chen, Qixin ; Xia, Kaishun ; Wang, Chenggui ; Ying, Liwei ; Shi, Kesi ; Cheng, Feng ; Wang, Jingkai ; Yang, Biao ; Zhang, Yuang ; Gong, Zhe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-c2faccda0922a35dd9c5f35044a9e7938ebec1673376be865d39cec3a2d202a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Apoptosis</topic><topic>Back pain</topic><topic>Biomarkers</topic><topic>Cell cycle</topic><topic>Cell division</topic><topic>Cell Survival - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Xianpeng</au><au>Yu, Chao</au><au>Li, Fangcai</au><au>Liang, Chengzhen</au><au>Chen, Qixin</au><au>Xia, Kaishun</au><au>Wang, Chenggui</au><au>Ying, Liwei</au><au>Shi, Kesi</au><au>Cheng, Feng</au><au>Wang, Jingkai</au><au>Yang, Biao</au><au>Zhang, Yuang</au><au>Gong, Zhe</au><au>Ding, Wenyuan</au><au>Wenyuan Ding</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell Senescence: A Nonnegligible Cell State under Survival Stress in Pathology of Intervertebral Disc Degeneration</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>The intervertebral disc degeneration (IDD) with increasing aging mainly manifests as low back pain (LBP) accompanied with a loss of physical ability. These pathological processes can be preliminarily interpreted as a series of changes at cellular level. In addition to cell death, disc cells enter into the stagnation with dysfunction and deteriorate tissue microenvironment in degenerative discs, which is recognized as cell senescence. During aging, many intrinsic and extrinsic factors have been proved to have strong connections with these cellular senescence phenomena. Growing evidences of these connections require us to gather up critical cues from potential risk factors to pathogenesis and relative interventions for retarding cell senescence and attenuating degenerative changes. In this paper, we try to clarify another important cell state apart from cell death in IDD and discuss senescence-associated changes in cells and extracellular microenvironment. Then, we emphasize the role of oxidative stress and epigenomic perturbations in linking risk factors to cell senescence in the onset of IDD. Further, we summarize the current interventions targeting senescent cells that may exert the benefits of antidegeneration in IDD.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32934764</pmid><doi>10.1155/2020/9503562</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-2626-0201</orcidid><orcidid>https://orcid.org/0000-0002-4983-6461</orcidid><orcidid>https://orcid.org/0000-0002-2402-781X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Aging Apoptosis Back pain Biomarkers Cell cycle Cell division Cell Survival - genetics Cellular Microenvironment - genetics Cellular Senescence - genetics Chronic illnesses Deoxyribonucleic acid DNA DNA damage Epigenesis, Genetic Epigenetics Gene expression Growth factors Humans Intervertebral Disc Degeneration - genetics Intervertebral Disc Degeneration - pathology Intervertebral Disc Degeneration - therapy Kinases Oxidative Stress - genetics Review Senescence |
title | Cell Senescence: A Nonnegligible Cell State under Survival Stress in Pathology of Intervertebral Disc Degeneration |
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