Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway
Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of myocardi...
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| description | Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of myocardial survival induced by tilianin, a flavonoid antioxidant. Tilianin (2.5, 5, and 10 mg/kg/d) or saline was orally administered to rats for 14 days. On the 15th day, ischemia was induced by ligating the left anterior descending artery for 45 min, followed by 4 h of reperfusion. The levels of MIRI-induced serum myocardial enzymes and cardiomyocyte apoptosis as well as infarct size were examined to assess the cardioprotective effects. Cardiac tissues were collected for western blot analyses to determine the protein expression of anti-apoptotic signaling molecules. In MIRI-treated rats, our results revealed that pre-administration of high dose-tilianin the reduced release of LDH, MDA, and CK-MB and increased the plasma SOD level, and significantly attenuated the infarct size. Western blot analysis showed that a remarkable rise in expression of Bcl-2 and XIAP, and decline in expression of Bax, Smac/Diablo, HtrA2/Omi, cleaved caspase-3, caspase-7 and caspase-9 was observed in the myocardium. The apoptosis index of cardiomyocytes further supports the cardioprotective effect of tilianin. Additionally, compared with the MIRI model group, pretreatment with high dose-tilianin group upregulated phosphorylated Akt and PI3K. In contrast, using the PI3K inhibitor LY294002 to block Akt activation effectively inhibited the protective effects of tilianin against MIRI. Tilianin pretreatment was beneficial for activating the PI3K/Akt signaling pathway and inhibiting myocardial apoptosis. |
| doi_str_mv | 10.1371/journal.pone.0193845 |
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Our study aimed to investigate the molecular signaling implicated in the improvement of myocardial survival induced by tilianin, a flavonoid antioxidant. Tilianin (2.5, 5, and 10 mg/kg/d) or saline was orally administered to rats for 14 days. On the 15th day, ischemia was induced by ligating the left anterior descending artery for 45 min, followed by 4 h of reperfusion. The levels of MIRI-induced serum myocardial enzymes and cardiomyocyte apoptosis as well as infarct size were examined to assess the cardioprotective effects. Cardiac tissues were collected for western blot analyses to determine the protein expression of anti-apoptotic signaling molecules. In MIRI-treated rats, our results revealed that pre-administration of high dose-tilianin the reduced release of LDH, MDA, and CK-MB and increased the plasma SOD level, and significantly attenuated the infarct size. Western blot analysis showed that a remarkable rise in expression of Bcl-2 and XIAP, and decline in expression of Bax, Smac/Diablo, HtrA2/Omi, cleaved caspase-3, caspase-7 and caspase-9 was observed in the myocardium. The apoptosis index of cardiomyocytes further supports the cardioprotective effect of tilianin. Additionally, compared with the MIRI model group, pretreatment with high dose-tilianin group upregulated phosphorylated Akt and PI3K. In contrast, using the PI3K inhibitor LY294002 to block Akt activation effectively inhibited the protective effects of tilianin against MIRI. Tilianin pretreatment was beneficial for activating the PI3K/Akt signaling pathway and inhibiting myocardial apoptosis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0193845</identifier><identifier>PMID: 29538428</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; Administration, Oral ; AKT protein ; Animal tissues ; Animals ; Antioxidants ; Apoptosis ; Apoptosis - physiology ; Bax protein ; Bcl-2 protein ; Biology and Life Sciences ; Cardiomyocytes ; Cardiotonic Agents - chemistry ; Cardiotonic Agents - pharmacology ; Cardiovascular disease ; Caspase ; Caspase-3 ; Caspase-7 ; Caspase-9 ; Chromones - pharmacology ; DIABLO protein ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Dracocephalum moldavica ; Drugs, Chinese Herbal ; Enzyme Inhibitors - pharmacology ; Flavonoids - chemistry ; Flavonoids - pharmacology ; Glycosides - chemistry ; Glycosides - pharmacology ; Heart diseases ; Ischemia ; Kinases ; Male ; Medicine and Health Sciences ; Molecular Structure ; Morpholines - pharmacology ; Myocardial ischemia ; Myocardial Reperfusion Injury - diagnostic imaging ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardium ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Oral administration ; Pharmacology ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors ; Proto-Oncogene Proteins c-akt - metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Reperfusion injury ; Rodents ; Signal Transduction ; Signaling ; XIAP protein</subject><ispartof>PloS one, 2018-03, Vol.13 (3), p.e0193845-e0193845</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Zeng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 Zeng et al 2018 Zeng et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-2b0987beadef2e1383560bc628e001ffc8eea6e4f39007dd694ba6e4296c12283</citedby><cites>FETCH-LOGICAL-c758t-2b0987beadef2e1383560bc628e001ffc8eea6e4f39007dd694ba6e4296c12283</cites><orcidid>0000-0002-5711-5664</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/PMC5851616/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5851616/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29538428$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Cheng</creatorcontrib><creatorcontrib>Jiang, Wen</creatorcontrib><creatorcontrib>Zheng, Ruifang</creatorcontrib><creatorcontrib>He, Chenghui</creatorcontrib><creatorcontrib>Li, Jianguang</creatorcontrib><creatorcontrib>Xing, Jianguo</creatorcontrib><title>Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of myocardial survival induced by tilianin, a flavonoid antioxidant. Tilianin (2.5, 5, and 10 mg/kg/d) or saline was orally administered to rats for 14 days. On the 15th day, ischemia was induced by ligating the left anterior descending artery for 45 min, followed by 4 h of reperfusion. The levels of MIRI-induced serum myocardial enzymes and cardiomyocyte apoptosis as well as infarct size were examined to assess the cardioprotective effects. Cardiac tissues were collected for western blot analyses to determine the protein expression of anti-apoptotic signaling molecules. In MIRI-treated rats, our results revealed that pre-administration of high dose-tilianin the reduced release of LDH, MDA, and CK-MB and increased the plasma SOD level, and significantly attenuated the infarct size. Western blot analysis showed that a remarkable rise in expression of Bcl-2 and XIAP, and decline in expression of Bax, Smac/Diablo, HtrA2/Omi, cleaved caspase-3, caspase-7 and caspase-9 was observed in the myocardium. The apoptosis index of cardiomyocytes further supports the cardioprotective effect of tilianin. Additionally, compared with the MIRI model group, pretreatment with high dose-tilianin group upregulated phosphorylated Akt and PI3K. In contrast, using the PI3K inhibitor LY294002 to block Akt activation effectively inhibited the protective effects of tilianin against MIRI. Tilianin pretreatment was beneficial for activating the PI3K/Akt signaling pathway and inhibiting myocardial apoptosis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Administration, Oral</subject><subject>AKT protein</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>Biology and Life Sciences</subject><subject>Cardiomyocytes</subject><subject>Cardiotonic Agents - chemistry</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cardiovascular disease</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-7</subject><subject>Caspase-9</subject><subject>Chromones - pharmacology</subject><subject>DIABLO protein</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Dracocephalum moldavica</subject><subject>Drugs, Chinese Herbal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Flavonoids - chemistry</subject><subject>Flavonoids - pharmacology</subject><subject>Glycosides - chemistry</subject><subject>Glycosides - pharmacology</subject><subject>Heart diseases</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Molecular Structure</subject><subject>Morpholines - pharmacology</subject><subject>Myocardial ischemia</subject><subject>Myocardial Reperfusion Injury - diagnostic imaging</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardium</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Oral administration</subject><subject>Pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion</subject><subject>Reperfusion injury</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>XIAP protein</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1lv1DAQxyMEomXhGyCIhITgYRcfOXlAqlYcK1WqVI5Xy3HGiVdOnNoOdL89TjetGtQHlIdMnN_85_BMFL3EaINpjj_szWh7rjeD6WGDcEmLJH0UnQaDrDOC6ON79kn0zLk9QiktsuxpdELKYCWkOI2ut9zWygzWeBBemT42MvZKK96rPuYdaGUs9-Di7mDExHIdKyda6BRfWxjAytFNfqrfj_bwMb40Gm5EWoj5YAZvvBKxU01IVvVNPHDf_uGH59ETybWDF_N7Ff388vnH9tv6_OLrbnt2vhZ5Wvg1qVBZ5BXwGiQBTAuaZqgSGSkAISylKAB4BomkJUJ5XWdlUk3fpMwEJqSgq-j1UXfQxrG5aY4RhBNM8pJmgdgdidrwPRus6rg9MMMVuzkwtmHchho0MFpJkco8r6cQGaUFL3OaVmlSZymGUgatT3O0seqgFtB7y_VCdPmnVy1rzG-WFinO8JTMu1nAmqsRnGdd6DZozXsw45x3QktSBvTNP-jD1c1Uw0MBqpcmxBWTKDtLKUZhKMIwrKLNA1R46nDPIkyYVOF84fB-4RAYD9e-4aNzbPf98v_Zi19L9u09tgWufeuMHqfRdEswOYLCGucsyLsmY8SmBbntBpsWhM0LEtxe3b-gO6fbjaB_AVIiDXI</recordid><startdate>20180314</startdate><enddate>20180314</enddate><creator>Zeng, Cheng</creator><creator>Jiang, Wen</creator><creator>Zheng, Ruifang</creator><creator>He, Chenghui</creator><creator>Li, Jianguang</creator><creator>Xing, Jianguo</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-5711-5664</orcidid></search><sort><creationdate>20180314</creationdate><title>Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway</title><author>Zeng, Cheng ; Jiang, Wen ; Zheng, Ruifang ; He, Chenghui ; Li, Jianguang ; Xing, Jianguo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-2b0987beadef2e1383560bc628e001ffc8eea6e4f39007dd694ba6e4296c12283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Administration, Oral</topic><topic>AKT protein</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>Biology and Life Sciences</topic><topic>Cardiomyocytes</topic><topic>Cardiotonic Agents - chemistry</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cardiovascular disease</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-7</topic><topic>Caspase-9</topic><topic>Chromones - pharmacology</topic><topic>DIABLO protein</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Dracocephalum moldavica</topic><topic>Drugs, Chinese Herbal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Flavonoids - chemistry</topic><topic>Flavonoids - pharmacology</topic><topic>Glycosides - chemistry</topic><topic>Glycosides - pharmacology</topic><topic>Heart diseases</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Male</topic><topic>Medicine and Health Sciences</topic><topic>Molecular Structure</topic><topic>Morpholines - pharmacology</topic><topic>Myocardial ischemia</topic><topic>Myocardial Reperfusion Injury - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Cheng</au><au>Jiang, Wen</au><au>Zheng, Ruifang</au><au>He, Chenghui</au><au>Li, Jianguang</au><au>Xing, Jianguo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2018-03-14</date><risdate>2018</risdate><volume>13</volume><issue>3</issue><spage>e0193845</spage><epage>e0193845</epage><pages>e0193845-e0193845</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of myocardial survival induced by tilianin, a flavonoid antioxidant. Tilianin (2.5, 5, and 10 mg/kg/d) or saline was orally administered to rats for 14 days. On the 15th day, ischemia was induced by ligating the left anterior descending artery for 45 min, followed by 4 h of reperfusion. The levels of MIRI-induced serum myocardial enzymes and cardiomyocyte apoptosis as well as infarct size were examined to assess the cardioprotective effects. Cardiac tissues were collected for western blot analyses to determine the protein expression of anti-apoptotic signaling molecules. In MIRI-treated rats, our results revealed that pre-administration of high dose-tilianin the reduced release of LDH, MDA, and CK-MB and increased the plasma SOD level, and significantly attenuated the infarct size. Western blot analysis showed that a remarkable rise in expression of Bcl-2 and XIAP, and decline in expression of Bax, Smac/Diablo, HtrA2/Omi, cleaved caspase-3, caspase-7 and caspase-9 was observed in the myocardium. The apoptosis index of cardiomyocytes further supports the cardioprotective effect of tilianin. Additionally, compared with the MIRI model group, pretreatment with high dose-tilianin group upregulated phosphorylated Akt and PI3K. In contrast, using the PI3K inhibitor LY294002 to block Akt activation effectively inhibited the protective effects of tilianin against MIRI. Tilianin pretreatment was beneficial for activating the PI3K/Akt signaling pathway and inhibiting myocardial apoptosis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29538428</pmid><doi>10.1371/journal.pone.0193845</doi><tpages>e0193845</tpages><orcidid>https://orcid.org/0000-0002-5711-5664</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_2014127936 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Phosphatidylinositol 3-kinase Administration, Oral AKT protein Animal tissues Animals Antioxidants Apoptosis Apoptosis - physiology Bax protein Bcl-2 protein Biology and Life Sciences Cardiomyocytes Cardiotonic Agents - chemistry Cardiotonic Agents - pharmacology Cardiovascular disease Caspase Caspase-3 Caspase-7 Caspase-9 Chromones - pharmacology DIABLO protein Disease Models, Animal Dose-Response Relationship, Drug Dracocephalum moldavica Drugs, Chinese Herbal Enzyme Inhibitors - pharmacology Flavonoids - chemistry Flavonoids - pharmacology Glycosides - chemistry Glycosides - pharmacology Heart diseases Ischemia Kinases Male Medicine and Health Sciences Molecular Structure Morpholines - pharmacology Myocardial ischemia Myocardial Reperfusion Injury - diagnostic imaging Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardium Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Oral administration Pharmacology Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - metabolism Random Allocation Rats Rats, Sprague-Dawley Reperfusion Reperfusion injury Rodents Signal Transduction Signaling XIAP protein |
| title | Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T01%3A19%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cardioprotection%20of%20tilianin%20ameliorates%20myocardial%20ischemia-reperfusion%20injury:%20Role%20of%20the%20apoptotic%20signaling%20pathway&rft.jtitle=PloS%20one&rft.au=Zeng,%20Cheng&rft.date=2018-03-14&rft.volume=13&rft.issue=3&rft.spage=e0193845&rft.epage=e0193845&rft.pages=e0193845-e0193845&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0193845&rft_dat=%3Cgale_plos_%3EA531000595%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2014127936&rft_id=info:pmid/29538428&rft_galeid=A531000595&rft_doaj_id=oai_doaj_org_article_3bfc5f77da6e46338a9735b54d651e9f&rfr_iscdi=true |