l-Carnitine inhibits the senescence-associated secretory phenotype of aging adipose tissue by JNK/p53 pathway
Senescence-associated secretory phenotype (SASP) plays a role in aging adipose tissue dysfunction by directly promoting chronic inflammation. The JNK/p53 pathway was reported as a potential mechanism that mediates SASP. In this study, we investigated the effects of l -carnitine, an inhibitor of the...
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| Veröffentlicht in: | Biogerontology (Dordrecht) 2019-04, Vol.20 (2), p.203-211 |
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| creator | Yang, Lian-wei Song, Ming Li, Yu-lin Liu, Ya-peng Liu, Chun Han, Lu Wang, Zhi-hao Zhang, Wei Xing, Yan-qiu Zhong, Ming |
| description | Senescence-associated secretory phenotype (SASP) plays a role in aging adipose tissue dysfunction by directly promoting chronic inflammation. The JNK/p53 pathway was reported as a potential mechanism that mediates SASP. In this study, we investigated the effects of
l
-carnitine, an inhibitor of the JNK/p53 pathway in adipose tissue SASP and dysfunction. Young and aging rat were given
l
-carnitine by gavage. Next, we detected the senescence, cytokines expression, chronic inflammation and insulin resistance of adipose tissue. Additionally, JNK/p53 pathway was estimated. Our results show a significant increase expression of SASP components in the adipose tissue of aging rats compared to young rats. Further, we found that infiltration of immune cells and the expression of pro-inflammatory cytokines were enhanced in aging adipose tissue while insulin signaling activity was reduced in aging adipose tissue. Interestingly,
l
-carnitine markedly reduced the expression of SASP factors.
l
-Carnitine could significantly reduce chronic inflammation, improving insulin resistance. Further,
l
-carnitine inhibited SASP by inhibiting JNK/p53 pathway.
l
-Carnitine inhibited SASP by JNK/p53 pathway and attenuated adipose tissue dysfunction of aging. |
| doi_str_mv | 10.1007/s10522-018-9787-z |
| format | Article |
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l
-carnitine, an inhibitor of the JNK/p53 pathway in adipose tissue SASP and dysfunction. Young and aging rat were given
l
-carnitine by gavage. Next, we detected the senescence, cytokines expression, chronic inflammation and insulin resistance of adipose tissue. Additionally, JNK/p53 pathway was estimated. Our results show a significant increase expression of SASP components in the adipose tissue of aging rats compared to young rats. Further, we found that infiltration of immune cells and the expression of pro-inflammatory cytokines were enhanced in aging adipose tissue while insulin signaling activity was reduced in aging adipose tissue. Interestingly,
l
-carnitine markedly reduced the expression of SASP factors.
l
-Carnitine could significantly reduce chronic inflammation, improving insulin resistance. Further,
l
-carnitine inhibited SASP by inhibiting JNK/p53 pathway.
l
-Carnitine inhibited SASP by JNK/p53 pathway and attenuated adipose tissue dysfunction of aging.</description><identifier>ISSN: 1389-5729</identifier><identifier>EISSN: 1573-6768</identifier><identifier>DOI: 10.1007/s10522-018-9787-z</identifier><identifier>PMID: 30519860</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adipose tissue ; Aging ; Biomedical and Life Sciences ; Carnitine ; Cell Biology ; Cytokines ; Developmental Biology ; Geriatrics/Gerontology ; Inflammation ; Insulin ; Insulin resistance ; L-Carnitine ; Life Sciences ; p53 Protein ; Phenotypes ; Research Article ; Senescence</subject><ispartof>Biogerontology (Dordrecht), 2019-04, Vol.20 (2), p.203-211</ispartof><rights>Springer Nature B.V. 2018</rights><rights>Biogerontology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-8778d6c5aeedd1937eec576c4288f74b45f8ab5f31484cbd75cf8331c443276d3</citedby><cites>FETCH-LOGICAL-c372t-8778d6c5aeedd1937eec576c4288f74b45f8ab5f31484cbd75cf8331c443276d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10522-018-9787-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10522-018-9787-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30519860$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Lian-wei</creatorcontrib><creatorcontrib>Song, Ming</creatorcontrib><creatorcontrib>Li, Yu-lin</creatorcontrib><creatorcontrib>Liu, Ya-peng</creatorcontrib><creatorcontrib>Liu, Chun</creatorcontrib><creatorcontrib>Han, Lu</creatorcontrib><creatorcontrib>Wang, Zhi-hao</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Xing, Yan-qiu</creatorcontrib><creatorcontrib>Zhong, Ming</creatorcontrib><title>l-Carnitine inhibits the senescence-associated secretory phenotype of aging adipose tissue by JNK/p53 pathway</title><title>Biogerontology (Dordrecht)</title><addtitle>Biogerontology</addtitle><addtitle>Biogerontology</addtitle><description>Senescence-associated secretory phenotype (SASP) plays a role in aging adipose tissue dysfunction by directly promoting chronic inflammation. The JNK/p53 pathway was reported as a potential mechanism that mediates SASP. In this study, we investigated the effects of
l
-carnitine, an inhibitor of the JNK/p53 pathway in adipose tissue SASP and dysfunction. Young and aging rat were given
l
-carnitine by gavage. Next, we detected the senescence, cytokines expression, chronic inflammation and insulin resistance of adipose tissue. Additionally, JNK/p53 pathway was estimated. Our results show a significant increase expression of SASP components in the adipose tissue of aging rats compared to young rats. Further, we found that infiltration of immune cells and the expression of pro-inflammatory cytokines were enhanced in aging adipose tissue while insulin signaling activity was reduced in aging adipose tissue. Interestingly,
l
-carnitine markedly reduced the expression of SASP factors.
l
-Carnitine could significantly reduce chronic inflammation, improving insulin resistance. Further,
l
-carnitine inhibited SASP by inhibiting JNK/p53 pathway.
l
-Carnitine inhibited SASP by JNK/p53 pathway and attenuated adipose tissue dysfunction of aging.</description><subject>Adipose tissue</subject><subject>Aging</subject><subject>Biomedical and Life Sciences</subject><subject>Carnitine</subject><subject>Cell Biology</subject><subject>Cytokines</subject><subject>Developmental Biology</subject><subject>Geriatrics/Gerontology</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>L-Carnitine</subject><subject>Life Sciences</subject><subject>p53 Protein</subject><subject>Phenotypes</subject><subject>Research Article</subject><subject>Senescence</subject><issn>1389-5729</issn><issn>1573-6768</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU1vFDEMhiMEoqXwA7igSFx6Cc3H5GOOaAWlUNFLOUeZjGc31W4yJBlV019Pqi0gIXGyZT9-E_tF6C2jHxil-qIwKjknlBnSa6PJwzN0yqQWRGllnrdcmJ5IzfsT9KqUO0qZ4kq-RCeCStYbRU_RYU82LsdQQwQc4i4MoRZcd4ALRCgeogfiSkk-uApjq_oMNeUVzzuIqa4z4DRhtw1xi90Y5lQA11DKAnhY8dfv3y5mKfDs6u7era_Ri8ntC7x5imfox-dPt5sv5Prm8mrz8Zp4oXklRmszKi8dwDiyXmgAL7XyHTdm0t3Qycm4QU6Cdabzw6iln4wQzHed4FqN4gydH3XnnH4uUKo9hLbLfu8ipKVYznTPhVCKNfT9P-hdWnJsv2uUpFxwJvpGsSPlcyolw2TnHA4ur5ZR--iFPXphmxf20Qv70GbePSkvwwHGPxO_j98AfgRKa8Ut5L9P_1_1F9uolWU</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Yang, Lian-wei</creator><creator>Song, Ming</creator><creator>Li, Yu-lin</creator><creator>Liu, Ya-peng</creator><creator>Liu, Chun</creator><creator>Han, Lu</creator><creator>Wang, Zhi-hao</creator><creator>Zhang, Wei</creator><creator>Xing, Yan-qiu</creator><creator>Zhong, Ming</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88J</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2R</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20190401</creationdate><title>l-Carnitine inhibits the senescence-associated secretory phenotype of aging adipose tissue by JNK/p53 pathway</title><author>Yang, Lian-wei ; Song, Ming ; Li, Yu-lin ; Liu, Ya-peng ; Liu, Chun ; Han, Lu ; Wang, Zhi-hao ; Zhang, Wei ; Xing, Yan-qiu ; Zhong, Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-8778d6c5aeedd1937eec576c4288f74b45f8ab5f31484cbd75cf8331c443276d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adipose tissue</topic><topic>Aging</topic><topic>Biomedical and Life Sciences</topic><topic>Carnitine</topic><topic>Cell Biology</topic><topic>Cytokines</topic><topic>Developmental Biology</topic><topic>Geriatrics/Gerontology</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>L-Carnitine</topic><topic>Life Sciences</topic><topic>p53 Protein</topic><topic>Phenotypes</topic><topic>Research Article</topic><topic>Senescence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Lian-wei</creatorcontrib><creatorcontrib>Song, Ming</creatorcontrib><creatorcontrib>Li, Yu-lin</creatorcontrib><creatorcontrib>Liu, Ya-peng</creatorcontrib><creatorcontrib>Liu, Chun</creatorcontrib><creatorcontrib>Han, Lu</creatorcontrib><creatorcontrib>Wang, Zhi-hao</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Xing, Yan-qiu</creatorcontrib><creatorcontrib>Zhong, Ming</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Social Science Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Biogerontology (Dordrecht)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Lian-wei</au><au>Song, Ming</au><au>Li, Yu-lin</au><au>Liu, Ya-peng</au><au>Liu, Chun</au><au>Han, Lu</au><au>Wang, Zhi-hao</au><au>Zhang, Wei</au><au>Xing, Yan-qiu</au><au>Zhong, Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>l-Carnitine inhibits the senescence-associated secretory phenotype of aging adipose tissue by JNK/p53 pathway</atitle><jtitle>Biogerontology (Dordrecht)</jtitle><stitle>Biogerontology</stitle><addtitle>Biogerontology</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>20</volume><issue>2</issue><spage>203</spage><epage>211</epage><pages>203-211</pages><issn>1389-5729</issn><eissn>1573-6768</eissn><abstract>Senescence-associated secretory phenotype (SASP) plays a role in aging adipose tissue dysfunction by directly promoting chronic inflammation. The JNK/p53 pathway was reported as a potential mechanism that mediates SASP. In this study, we investigated the effects of
l
-carnitine, an inhibitor of the JNK/p53 pathway in adipose tissue SASP and dysfunction. Young and aging rat were given
l
-carnitine by gavage. Next, we detected the senescence, cytokines expression, chronic inflammation and insulin resistance of adipose tissue. Additionally, JNK/p53 pathway was estimated. Our results show a significant increase expression of SASP components in the adipose tissue of aging rats compared to young rats. Further, we found that infiltration of immune cells and the expression of pro-inflammatory cytokines were enhanced in aging adipose tissue while insulin signaling activity was reduced in aging adipose tissue. Interestingly,
l
-carnitine markedly reduced the expression of SASP factors.
l
-Carnitine could significantly reduce chronic inflammation, improving insulin resistance. Further,
l
-carnitine inhibited SASP by inhibiting JNK/p53 pathway.
l
-Carnitine inhibited SASP by JNK/p53 pathway and attenuated adipose tissue dysfunction of aging.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>30519860</pmid><doi>10.1007/s10522-018-9787-z</doi><tpages>9</tpages></addata></record> |
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| subjects | Adipose tissue Aging Biomedical and Life Sciences Carnitine Cell Biology Cytokines Developmental Biology Geriatrics/Gerontology Inflammation Insulin Insulin resistance L-Carnitine Life Sciences p53 Protein Phenotypes Research Article Senescence |
| title | l-Carnitine inhibits the senescence-associated secretory phenotype of aging adipose tissue by JNK/p53 pathway |
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