Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway
Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms. Sesn2 expression was detected in aortas colle...
Gespeichert in:
| Veröffentlicht in: | Life sciences (1973) 2019-02, Vol.218, p.132-138 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 138 |
|---|---|
| container_issue | |
| container_start_page | 132 |
| container_title | Life sciences (1973) |
| container_volume | 218 |
| creator | Xiao, Ting Zhang, Le Huang, Ying Shi, Ying Wang, Jing Ji, Qingwei Ye, Jing Lin, Yingzhong Liu, Hongtao |
| description | Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms.
Sesn2 expression was detected in aortas collected from AD patients and normal donors. In addition, blood samples were collected from AD patients and non-AD (NAD) patients, and the plasma Sesn2 levels were measured. Furthermore, the effects of Sesn2 on angiotensin (Ang) II-induced smooth muscle cell (SMC) apoptosis were investigated in vitro.
Compared with the aortas from normal donors, aortas from AD patients had significantly increased Sesn2. Sesn2 was mainly secreted by macrophages, and low levels were secreted by CD4+ T lymphocytes, but not SMCs. Plasma Sesn2 levels were also increased in AD patients compared with NAD patients. Sesn2 levels were negatively corrected with superoxide dismutase (SOD) levels but positively corrected with malondialdehyde (MDA) levels in AD patients. In co-cultures of macrophages and SMCs, Sesn2 overexpression in macrophages significantly reduced Ang II-induced SMC apoptosis, and this effect could be reversed by Nrf2 silencing.
Sesn2 is increased in both aortas and plasma from AD patients. Sesn2 may alleviate Ang II-induced SMC apoptosis and participate in AD via the Nrf2 pathway. Sesn2 may be a new target in the treatment and prevention of AD. |
| doi_str_mv | 10.1016/j.lfs.2018.12.043 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2161924002</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0024320518308361</els_id><sourcerecordid>2161924002</sourcerecordid><originalsourceid>FETCH-LOGICAL-c447t-52064366695903fefed732d96b721d01aba1c1a77d27c2922cf9f9712db1e9b03</originalsourceid><addsrcrecordid>eNp9kb2O1DAURi0EYoeFB6BBlmhoEmwnsceiQqsFRlpBAdSWY98wHiVx8HUW7dPwqjjMQkFB5R-d--nqO4Q856zmjMvXp3ocsBaM72suatY2D8iO75WumGz4Q7JjTLRVI1h3QZ4gnhhjXaeax-SiYZ1upWx35OdnwJzCLGiYXQKLgOVGbUzZIrWzp8tocbJ0SHH6_R0c9QERXA5xpovNAeZ8Ru04wm2wGbbntxAzzFjCDocqzH514ClOMeYjnVZ0I1AH40jtEpccMSAtozQfgX5Mg9iCjz_s3VPyaLAjwrP785J8fXf95epDdfPp_eHq7U3l2lblqhNMto2UUneaNQMM4FUjvJa9EtwzbnvLHbdKeaGc0EK4QQ9aceF7DrpnzSV5dc5dUvy-lk7MFHDbz84QVzSCS65FWxot6Mt_0FNc01y2K9Seq07stS4UP1MuRcQEg1lSmGy6M5yZzZ45mWLPbPYMF6bYKzMv7pPXfgL_d-KPrgK8OQNQqrgNkAy6Un9pNqQixPgY_hP_C6h-rIw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2181752899</pqid></control><display><type>article</type><title>Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Xiao, Ting ; Zhang, Le ; Huang, Ying ; Shi, Ying ; Wang, Jing ; Ji, Qingwei ; Ye, Jing ; Lin, Yingzhong ; Liu, Hongtao</creator><creatorcontrib>Xiao, Ting ; Zhang, Le ; Huang, Ying ; Shi, Ying ; Wang, Jing ; Ji, Qingwei ; Ye, Jing ; Lin, Yingzhong ; Liu, Hongtao</creatorcontrib><description>Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms.
Sesn2 expression was detected in aortas collected from AD patients and normal donors. In addition, blood samples were collected from AD patients and non-AD (NAD) patients, and the plasma Sesn2 levels were measured. Furthermore, the effects of Sesn2 on angiotensin (Ang) II-induced smooth muscle cell (SMC) apoptosis were investigated in vitro.
Compared with the aortas from normal donors, aortas from AD patients had significantly increased Sesn2. Sesn2 was mainly secreted by macrophages, and low levels were secreted by CD4+ T lymphocytes, but not SMCs. Plasma Sesn2 levels were also increased in AD patients compared with NAD patients. Sesn2 levels were negatively corrected with superoxide dismutase (SOD) levels but positively corrected with malondialdehyde (MDA) levels in AD patients. In co-cultures of macrophages and SMCs, Sesn2 overexpression in macrophages significantly reduced Ang II-induced SMC apoptosis, and this effect could be reversed by Nrf2 silencing.
Sesn2 is increased in both aortas and plasma from AD patients. Sesn2 may alleviate Ang II-induced SMC apoptosis and participate in AD via the Nrf2 pathway. Sesn2 may be a new target in the treatment and prevention of AD.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2018.12.043</identifier><identifier>PMID: 30594664</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Aneurysm, Dissecting ; Angiotensin ; Angiotensin II ; Angiotensin II - pharmacology ; Antioxidants ; Aorta ; Aorta - drug effects ; Aorta - metabolism ; Aorta - pathology ; Aortic Diseases - metabolism ; Aortic Diseases - pathology ; Aortic Diseases - surgery ; Aortic dissection ; Apoptosis ; Biomarkers - metabolism ; Case-Control Studies ; CD4 antigen ; Cell Proliferation ; Cells, Cultured ; Dissection ; Female ; Health risk assessment ; Humans ; Lymphocytes ; Lymphocytes T ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Macrophages - pathology ; Male ; Malondialdehyde ; Middle Aged ; Muscles ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - pathology ; NAD ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oxidative Stress ; Patients ; Plasma ; Proteins ; Sestrin2 ; Smooth muscle ; Smooth muscle cells ; Superoxide dismutase ; Vasoconstrictor Agents - pharmacology</subject><ispartof>Life sciences (1973), 2019-02, Vol.218, p.132-138</ispartof><rights>2018</rights><rights>Copyright © 2018. Published by Elsevier Inc.</rights><rights>Copyright Elsevier BV Feb 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-52064366695903fefed732d96b721d01aba1c1a77d27c2922cf9f9712db1e9b03</citedby><cites>FETCH-LOGICAL-c447t-52064366695903fefed732d96b721d01aba1c1a77d27c2922cf9f9712db1e9b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2018.12.043$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30594664$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Ting</creatorcontrib><creatorcontrib>Zhang, Le</creatorcontrib><creatorcontrib>Huang, Ying</creatorcontrib><creatorcontrib>Shi, Ying</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Ji, Qingwei</creatorcontrib><creatorcontrib>Ye, Jing</creatorcontrib><creatorcontrib>Lin, Yingzhong</creatorcontrib><creatorcontrib>Liu, Hongtao</creatorcontrib><title>Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms.
Sesn2 expression was detected in aortas collected from AD patients and normal donors. In addition, blood samples were collected from AD patients and non-AD (NAD) patients, and the plasma Sesn2 levels were measured. Furthermore, the effects of Sesn2 on angiotensin (Ang) II-induced smooth muscle cell (SMC) apoptosis were investigated in vitro.
Compared with the aortas from normal donors, aortas from AD patients had significantly increased Sesn2. Sesn2 was mainly secreted by macrophages, and low levels were secreted by CD4+ T lymphocytes, but not SMCs. Plasma Sesn2 levels were also increased in AD patients compared with NAD patients. Sesn2 levels were negatively corrected with superoxide dismutase (SOD) levels but positively corrected with malondialdehyde (MDA) levels in AD patients. In co-cultures of macrophages and SMCs, Sesn2 overexpression in macrophages significantly reduced Ang II-induced SMC apoptosis, and this effect could be reversed by Nrf2 silencing.
Sesn2 is increased in both aortas and plasma from AD patients. Sesn2 may alleviate Ang II-induced SMC apoptosis and participate in AD via the Nrf2 pathway. Sesn2 may be a new target in the treatment and prevention of AD.</description><subject>Aneurysm, Dissecting</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Antioxidants</subject><subject>Aorta</subject><subject>Aorta - drug effects</subject><subject>Aorta - metabolism</subject><subject>Aorta - pathology</subject><subject>Aortic Diseases - metabolism</subject><subject>Aortic Diseases - pathology</subject><subject>Aortic Diseases - surgery</subject><subject>Aortic dissection</subject><subject>Apoptosis</subject><subject>Biomarkers - metabolism</subject><subject>Case-Control Studies</subject><subject>CD4 antigen</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Dissection</subject><subject>Female</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Middle Aged</subject><subject>Muscles</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>NAD</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oxidative Stress</subject><subject>Patients</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Sestrin2</subject><subject>Smooth muscle</subject><subject>Smooth muscle cells</subject><subject>Superoxide dismutase</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kb2O1DAURi0EYoeFB6BBlmhoEmwnsceiQqsFRlpBAdSWY98wHiVx8HUW7dPwqjjMQkFB5R-d--nqO4Q856zmjMvXp3ocsBaM72suatY2D8iO75WumGz4Q7JjTLRVI1h3QZ4gnhhjXaeax-SiYZ1upWx35OdnwJzCLGiYXQKLgOVGbUzZIrWzp8tocbJ0SHH6_R0c9QERXA5xpovNAeZ8Ru04wm2wGbbntxAzzFjCDocqzH514ClOMeYjnVZ0I1AH40jtEpccMSAtozQfgX5Mg9iCjz_s3VPyaLAjwrP785J8fXf95epDdfPp_eHq7U3l2lblqhNMto2UUneaNQMM4FUjvJa9EtwzbnvLHbdKeaGc0EK4QQ9aceF7DrpnzSV5dc5dUvy-lk7MFHDbz84QVzSCS65FWxot6Mt_0FNc01y2K9Seq07stS4UP1MuRcQEg1lSmGy6M5yZzZ45mWLPbPYMF6bYKzMv7pPXfgL_d-KPrgK8OQNQqrgNkAy6Un9pNqQixPgY_hP_C6h-rIw</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Xiao, Ting</creator><creator>Zhang, Le</creator><creator>Huang, Ying</creator><creator>Shi, Ying</creator><creator>Wang, Jing</creator><creator>Ji, Qingwei</creator><creator>Ye, Jing</creator><creator>Lin, Yingzhong</creator><creator>Liu, Hongtao</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20190201</creationdate><title>Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway</title><author>Xiao, Ting ; Zhang, Le ; Huang, Ying ; Shi, Ying ; Wang, Jing ; Ji, Qingwei ; Ye, Jing ; Lin, Yingzhong ; Liu, Hongtao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-52064366695903fefed732d96b721d01aba1c1a77d27c2922cf9f9712db1e9b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aneurysm, Dissecting</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Antioxidants</topic><topic>Aorta</topic><topic>Aorta - drug effects</topic><topic>Aorta - metabolism</topic><topic>Aorta - pathology</topic><topic>Aortic Diseases - metabolism</topic><topic>Aortic Diseases - pathology</topic><topic>Aortic Diseases - surgery</topic><topic>Aortic dissection</topic><topic>Apoptosis</topic><topic>Biomarkers - metabolism</topic><topic>Case-Control Studies</topic><topic>CD4 antigen</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Dissection</topic><topic>Female</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Middle Aged</topic><topic>Muscles</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Myocytes, Smooth Muscle - pathology</topic><topic>NAD</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Oxidative Stress</topic><topic>Patients</topic><topic>Plasma</topic><topic>Proteins</topic><topic>Sestrin2</topic><topic>Smooth muscle</topic><topic>Smooth muscle cells</topic><topic>Superoxide dismutase</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Ting</creatorcontrib><creatorcontrib>Zhang, Le</creatorcontrib><creatorcontrib>Huang, Ying</creatorcontrib><creatorcontrib>Shi, Ying</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Ji, Qingwei</creatorcontrib><creatorcontrib>Ye, Jing</creatorcontrib><creatorcontrib>Lin, Yingzhong</creatorcontrib><creatorcontrib>Liu, Hongtao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Ting</au><au>Zhang, Le</au><au>Huang, Ying</au><au>Shi, Ying</au><au>Wang, Jing</au><au>Ji, Qingwei</au><au>Ye, Jing</au><au>Lin, Yingzhong</au><au>Liu, Hongtao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>218</volume><spage>132</spage><epage>138</epage><pages>132-138</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms.
Sesn2 expression was detected in aortas collected from AD patients and normal donors. In addition, blood samples were collected from AD patients and non-AD (NAD) patients, and the plasma Sesn2 levels were measured. Furthermore, the effects of Sesn2 on angiotensin (Ang) II-induced smooth muscle cell (SMC) apoptosis were investigated in vitro.
Compared with the aortas from normal donors, aortas from AD patients had significantly increased Sesn2. Sesn2 was mainly secreted by macrophages, and low levels were secreted by CD4+ T lymphocytes, but not SMCs. Plasma Sesn2 levels were also increased in AD patients compared with NAD patients. Sesn2 levels were negatively corrected with superoxide dismutase (SOD) levels but positively corrected with malondialdehyde (MDA) levels in AD patients. In co-cultures of macrophages and SMCs, Sesn2 overexpression in macrophages significantly reduced Ang II-induced SMC apoptosis, and this effect could be reversed by Nrf2 silencing.
Sesn2 is increased in both aortas and plasma from AD patients. Sesn2 may alleviate Ang II-induced SMC apoptosis and participate in AD via the Nrf2 pathway. Sesn2 may be a new target in the treatment and prevention of AD.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>30594664</pmid><doi>10.1016/j.lfs.2018.12.043</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0024-3205 |
| ispartof | Life sciences (1973), 2019-02, Vol.218, p.132-138 |
| issn | 0024-3205 1879-0631 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2161924002 |
| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Aneurysm, Dissecting Angiotensin Angiotensin II Angiotensin II - pharmacology Antioxidants Aorta Aorta - drug effects Aorta - metabolism Aorta - pathology Aortic Diseases - metabolism Aortic Diseases - pathology Aortic Diseases - surgery Aortic dissection Apoptosis Biomarkers - metabolism Case-Control Studies CD4 antigen Cell Proliferation Cells, Cultured Dissection Female Health risk assessment Humans Lymphocytes Lymphocytes T Macrophages Macrophages - drug effects Macrophages - metabolism Macrophages - pathology Male Malondialdehyde Middle Aged Muscles Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology NAD NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Nuclear Proteins - genetics Nuclear Proteins - metabolism Oxidative Stress Patients Plasma Proteins Sestrin2 Smooth muscle Smooth muscle cells Superoxide dismutase Vasoconstrictor Agents - pharmacology |
| title | Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T02%3A26%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Sestrin2%20increases%20in%20aortas%20and%20plasma%20from%20aortic%20dissection%20patients%20and%20alleviates%20angiotensin%20II-induced%20smooth%20muscle%20cell%20apoptosis%20via%20the%20Nrf2%20pathway&rft.jtitle=Life%20sciences%20(1973)&rft.au=Xiao,%20Ting&rft.date=2019-02-01&rft.volume=218&rft.spage=132&rft.epage=138&rft.pages=132-138&rft.issn=0024-3205&rft.eissn=1879-0631&rft_id=info:doi/10.1016/j.lfs.2018.12.043&rft_dat=%3Cproquest_cross%3E2161924002%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2181752899&rft_id=info:pmid/30594664&rft_els_id=S0024320518308361&rfr_iscdi=true |