MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1
A critical mechanism in atrial fibrillation (AF) is cardiac autonomic nerve remodeling (ANR). MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Numerous miRNAs are involved in diseases of the nervous and cardiovascular systems. We aimed to...
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| creator | Zhang, Yujiao Zheng, Shaohua Geng, Yangyang Xue, Jiao Wang, Zhongsu Xie, Xinxing Wang, Jiangrong Zhang, Shuyu Hou, Yinglong |
| description | A critical mechanism in atrial fibrillation (AF) is cardiac autonomic nerve remodeling (ANR). MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Numerous miRNAs are involved in diseases of the nervous and cardiovascular systems.
We aimed to assess the underlying role of miRNAs in regulating cardiac ANR in AF by right atrial tachypacing (A-TP) in canines.
Following 4-week A-TP, the superior left ganglionated plexuses (SLGPs), which are embedded in the fat pads of the left atrium, were subjected to miRNA expression profiling to screen preferentially expressed miRNAs. Sixteen miRNAs showed significantly differential expression between the control and A-TP groups, including miR-206, miR-203, miR-224 and miR-137. In particular, we focused on miR-206, which was elevated ~10-fold in A-TP dogs. Forced expression of miR-206 through lentiviral infection based on A-TP in vivo significantly shortened the atrial effective refractory period (AERP) (81 ± 7 vs. 98 ± 7 ms, P < 0.05). Immunohistochemical analysis showed that the regeneration of nerves increased more than 2-fold by miR-206 overexpression (P < 0.01). The expression of superoxide dismutase 1 (SOD1) was repressed by miR-206 overexpression by Western blot and luciferase assay, indicative of SOD1 as a direct target of miR-206. Overexpression of miR-206 increased reactive oxygen species (ROS) levels in vitro and in vivo, whereas miR-206 silencing attenuated irradiation- or A-TP-induced ROS. Knockdown of SOD1 effectively abolished ROS reduction caused by miR-206 silencing.
Our results found the differential expression of miRNAs in response to ANR in AF and elucidated the important role of miR-206 by targeting SOD1. The study illustrated the novel molecular mechanism of ANR and indicated a potential therapeutic target for AF. |
| doi_str_mv | 10.1371/journal.pone.0122674 |
| format | Article |
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We aimed to assess the underlying role of miRNAs in regulating cardiac ANR in AF by right atrial tachypacing (A-TP) in canines.
Following 4-week A-TP, the superior left ganglionated plexuses (SLGPs), which are embedded in the fat pads of the left atrium, were subjected to miRNA expression profiling to screen preferentially expressed miRNAs. Sixteen miRNAs showed significantly differential expression between the control and A-TP groups, including miR-206, miR-203, miR-224 and miR-137. In particular, we focused on miR-206, which was elevated ~10-fold in A-TP dogs. Forced expression of miR-206 through lentiviral infection based on A-TP in vivo significantly shortened the atrial effective refractory period (AERP) (81 ± 7 vs. 98 ± 7 ms, P < 0.05). Immunohistochemical analysis showed that the regeneration of nerves increased more than 2-fold by miR-206 overexpression (P < 0.01). The expression of superoxide dismutase 1 (SOD1) was repressed by miR-206 overexpression by Western blot and luciferase assay, indicative of SOD1 as a direct target of miR-206. Overexpression of miR-206 increased reactive oxygen species (ROS) levels in vitro and in vivo, whereas miR-206 silencing attenuated irradiation- or A-TP-induced ROS. Knockdown of SOD1 effectively abolished ROS reduction caused by miR-206 silencing.
Our results found the differential expression of miRNAs in response to ANR in AF and elucidated the important role of miR-206 by targeting SOD1. The study illustrated the novel molecular mechanism of ANR and indicated a potential therapeutic target for AF.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0122674</identifier><identifier>PMID: 25816284</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Atrial fibrillation ; Atrial Fibrillation - genetics ; Atrial Fibrillation - physiopathology ; Atrial Fibrillation - veterinary ; Atrium ; Autonomic Pathways - physiopathology ; Cardiac arrhythmia ; Cardiology ; Cells, Cultured ; Collaboration ; Dog Diseases - genetics ; Dog Diseases - physiopathology ; Dogs ; Fibrillation ; Gene expression ; Gene Expression Profiling - methods ; Gene Expression Regulation ; Genomes ; Health aspects ; Heart ; Heart diseases ; Higher education ; Hospitals ; Irradiation ; Laboratory animals ; Medicine ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Molecular chains ; Nerves ; Oxidative stress ; Oxygen ; Pathogenesis ; Post-transcription ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Refractory period ; Regeneration ; Ribonucleic acid ; RNA ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Superoxide Dismutase-1 ; Superoxides ; Therapeutic applications</subject><ispartof>PloS one, 2015-03, Vol.10 (3), p.e0122674-e0122674</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Zhang 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>2015 Zhang et al 2015 Zhang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-1dcd5881bea649435f37a5c07fd0bb354efa816aaecc021fefedad4858162863</citedby><cites>FETCH-LOGICAL-c758t-1dcd5881bea649435f37a5c07fd0bb354efa816aaecc021fefedad4858162863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376950/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376950/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25816284$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gupta, Sudhiranjan</contributor><creatorcontrib>Zhang, Yujiao</creatorcontrib><creatorcontrib>Zheng, Shaohua</creatorcontrib><creatorcontrib>Geng, Yangyang</creatorcontrib><creatorcontrib>Xue, Jiao</creatorcontrib><creatorcontrib>Wang, Zhongsu</creatorcontrib><creatorcontrib>Xie, Xinxing</creatorcontrib><creatorcontrib>Wang, Jiangrong</creatorcontrib><creatorcontrib>Zhang, Shuyu</creatorcontrib><creatorcontrib>Hou, Yinglong</creatorcontrib><title>MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>A critical mechanism in atrial fibrillation (AF) is cardiac autonomic nerve remodeling (ANR). MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Numerous miRNAs are involved in diseases of the nervous and cardiovascular systems.
We aimed to assess the underlying role of miRNAs in regulating cardiac ANR in AF by right atrial tachypacing (A-TP) in canines.
Following 4-week A-TP, the superior left ganglionated plexuses (SLGPs), which are embedded in the fat pads of the left atrium, were subjected to miRNA expression profiling to screen preferentially expressed miRNAs. Sixteen miRNAs showed significantly differential expression between the control and A-TP groups, including miR-206, miR-203, miR-224 and miR-137. In particular, we focused on miR-206, which was elevated ~10-fold in A-TP dogs. Forced expression of miR-206 through lentiviral infection based on A-TP in vivo significantly shortened the atrial effective refractory period (AERP) (81 ± 7 vs. 98 ± 7 ms, P < 0.05). Immunohistochemical analysis showed that the regeneration of nerves increased more than 2-fold by miR-206 overexpression (P < 0.01). The expression of superoxide dismutase 1 (SOD1) was repressed by miR-206 overexpression by Western blot and luciferase assay, indicative of SOD1 as a direct target of miR-206. Overexpression of miR-206 increased reactive oxygen species (ROS) levels in vitro and in vivo, whereas miR-206 silencing attenuated irradiation- or A-TP-induced ROS. Knockdown of SOD1 effectively abolished ROS reduction caused by miR-206 silencing.
Our results found the differential expression of miRNAs in response to ANR in AF and elucidated the important role of miR-206 by targeting SOD1. The study illustrated the novel molecular mechanism of ANR and indicated a potential therapeutic target for AF.</description><subject>Analysis</subject><subject>Animals</subject><subject>Atrial fibrillation</subject><subject>Atrial Fibrillation - genetics</subject><subject>Atrial Fibrillation - physiopathology</subject><subject>Atrial Fibrillation - veterinary</subject><subject>Atrium</subject><subject>Autonomic Pathways - physiopathology</subject><subject>Cardiac arrhythmia</subject><subject>Cardiology</subject><subject>Cells, Cultured</subject><subject>Collaboration</subject><subject>Dog Diseases - genetics</subject><subject>Dog Diseases - physiopathology</subject><subject>Dogs</subject><subject>Fibrillation</subject><subject>Gene expression</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Higher education</subject><subject>Hospitals</subject><subject>Irradiation</subject><subject>Laboratory animals</subject><subject>Medicine</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Molecular chains</subject><subject>Nerves</subject><subject>Oxidative stress</subject><subject>Oxygen</subject><subject>Pathogenesis</subject><subject>Post-transcription</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Refractory period</subject><subject>Regeneration</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase-1</subject><subject>Superoxides</subject><subject>Therapeutic applications</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1tv0zAUxyMEYmPwDRBEQkLw0OJLbCc8IFXjVmlQqZt4tRznJPWU2p2dTOwT8LVx1mxq0B5QHhL7_M7_5NyS5CVGc0wF_nDpem9VO985C3OECeEie5Qc44KSGSeIPj74PkqehXCJEKM550-TI8JyzEmeHSd_fhjt3frnIt15V5vW2CZ1dao6b1Sb1qb0pm1VZ5xNjU21ssZC-JhuzXpGEE-3ruqjGUK0RhcbjI6Qr4zSqeo7Z9023ljw15B6iDTcRihv4qkZPIfT-eozfp48qVUb4MX4Pkkuvn65OP0-O1t9W54uzmZasLyb4UpXLM9xCYpnRUZZTYViGom6QmVJWQa1iqkpBVojgmuooVJVlu_z5fQkeb2X3bUuyLGEQWLOBWYFwXkklnuicupS7rzZKn8jnTLy9sL5RirfGd2CLJXgSFCOCyYyTHleE4GhZESUtMSKRa1PY7S-3EKlIdZItRPRqcWajWzctcyo4AVDUeDdKODdVQ-hk1sTNMSOWHD9_r8LzjKGI_rmH_Th7EaqUTEBY2sX4-pBVC6yCCAkyFCl-QNUfCqI7YzzFgcFpg7vJw6R6eB316g-BLk8X_8_u_o1Zd8esBtQbbcJru2HeQxTMNuDcZhD8FDfFxkjOazLXTXksC5yXJfo9uqwQfdOd_tB_wIIVxBY</recordid><startdate>20150327</startdate><enddate>20150327</enddate><creator>Zhang, Yujiao</creator><creator>Zheng, Shaohua</creator><creator>Geng, Yangyang</creator><creator>Xue, Jiao</creator><creator>Wang, Zhongsu</creator><creator>Xie, Xinxing</creator><creator>Wang, Jiangrong</creator><creator>Zhang, Shuyu</creator><creator>Hou, Yinglong</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>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150327</creationdate><title>MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1</title><author>Zhang, Yujiao ; Zheng, Shaohua ; Geng, Yangyang ; Xue, Jiao ; Wang, Zhongsu ; Xie, Xinxing ; Wang, Jiangrong ; Zhang, Shuyu ; Hou, Yinglong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-1dcd5881bea649435f37a5c07fd0bb354efa816aaecc021fefedad4858162863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Atrial fibrillation</topic><topic>Atrial Fibrillation - genetics</topic><topic>Atrial Fibrillation - physiopathology</topic><topic>Atrial Fibrillation - veterinary</topic><topic>Atrium</topic><topic>Autonomic Pathways - physiopathology</topic><topic>Cardiac arrhythmia</topic><topic>Cardiology</topic><topic>Cells, Cultured</topic><topic>Collaboration</topic><topic>Dog Diseases - genetics</topic><topic>Dog Diseases - physiopathology</topic><topic>Dogs</topic><topic>Fibrillation</topic><topic>Gene expression</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Higher education</topic><topic>Hospitals</topic><topic>Irradiation</topic><topic>Laboratory animals</topic><topic>Medicine</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Molecular chains</topic><topic>Nerves</topic><topic>Oxidative stress</topic><topic>Oxygen</topic><topic>Pathogenesis</topic><topic>Post-transcription</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - 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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>Zhang, Yujiao</au><au>Zheng, Shaohua</au><au>Geng, Yangyang</au><au>Xue, Jiao</au><au>Wang, Zhongsu</au><au>Xie, Xinxing</au><au>Wang, Jiangrong</au><au>Zhang, Shuyu</au><au>Hou, Yinglong</au><au>Gupta, Sudhiranjan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-03-27</date><risdate>2015</risdate><volume>10</volume><issue>3</issue><spage>e0122674</spage><epage>e0122674</epage><pages>e0122674-e0122674</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>A critical mechanism in atrial fibrillation (AF) is cardiac autonomic nerve remodeling (ANR). MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Numerous miRNAs are involved in diseases of the nervous and cardiovascular systems.
We aimed to assess the underlying role of miRNAs in regulating cardiac ANR in AF by right atrial tachypacing (A-TP) in canines.
Following 4-week A-TP, the superior left ganglionated plexuses (SLGPs), which are embedded in the fat pads of the left atrium, were subjected to miRNA expression profiling to screen preferentially expressed miRNAs. Sixteen miRNAs showed significantly differential expression between the control and A-TP groups, including miR-206, miR-203, miR-224 and miR-137. In particular, we focused on miR-206, which was elevated ~10-fold in A-TP dogs. Forced expression of miR-206 through lentiviral infection based on A-TP in vivo significantly shortened the atrial effective refractory period (AERP) (81 ± 7 vs. 98 ± 7 ms, P < 0.05). Immunohistochemical analysis showed that the regeneration of nerves increased more than 2-fold by miR-206 overexpression (P < 0.01). The expression of superoxide dismutase 1 (SOD1) was repressed by miR-206 overexpression by Western blot and luciferase assay, indicative of SOD1 as a direct target of miR-206. Overexpression of miR-206 increased reactive oxygen species (ROS) levels in vitro and in vivo, whereas miR-206 silencing attenuated irradiation- or A-TP-induced ROS. Knockdown of SOD1 effectively abolished ROS reduction caused by miR-206 silencing.
Our results found the differential expression of miRNAs in response to ANR in AF and elucidated the important role of miR-206 by targeting SOD1. The study illustrated the novel molecular mechanism of ANR and indicated a potential therapeutic target for AF.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25816284</pmid><doi>10.1371/journal.pone.0122674</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1667159218 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Analysis Animals Atrial fibrillation Atrial Fibrillation - genetics Atrial Fibrillation - physiopathology Atrial Fibrillation - veterinary Atrium Autonomic Pathways - physiopathology Cardiac arrhythmia Cardiology Cells, Cultured Collaboration Dog Diseases - genetics Dog Diseases - physiopathology Dogs Fibrillation Gene expression Gene Expression Profiling - methods Gene Expression Regulation Genomes Health aspects Heart Heart diseases Higher education Hospitals Irradiation Laboratory animals Medicine MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Molecular chains Nerves Oxidative stress Oxygen Pathogenesis Post-transcription Reactive oxygen species Reactive Oxygen Species - metabolism Refractory period Regeneration Ribonucleic acid RNA Superoxide dismutase Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxide Dismutase-1 Superoxides Therapeutic applications |
| title | MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T09%3A59%3A51IST&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=MicroRNA%20profiling%20of%20atrial%20fibrillation%20in%20canines:%20miR-206%20modulates%20intrinsic%20cardiac%20autonomic%20nerve%20remodeling%20by%20regulating%20SOD1&rft.jtitle=PloS%20one&rft.au=Zhang,%20Yujiao&rft.date=2015-03-27&rft.volume=10&rft.issue=3&rft.spage=e0122674&rft.epage=e0122674&rft.pages=e0122674-e0122674&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0122674&rft_dat=%3Cgale_plos_%3EA421800726%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=1667159218&rft_id=info:pmid/25816284&rft_galeid=A421800726&rft_doaj_id=oai_doaj_org_article_ba760736195741368f271eb527b3b1a5&rfr_iscdi=true |