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Endocrine Protection of Ischemic Myocardium by FGF21 from the Liver and Adipose Tissue
Myocardial ischemia, while causing cardiomyocyte injury, can activate innate protective processes, enhancing myocardial tolerance to ischemia. Such processes are present in not only the heart, but also remote organs. In this investigation, we demonstrated a cardioprotective process involving FGF21 f...
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| Published in: | Scientific reports 2013-09, Vol.3 (1), p.2767-2767, Article 2767 |
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| creator | Liu, Shu Q. Roberts, Derek Kharitonenkov, Alexei Zhang, Brian Hanson, Samuel M. Li, Yan Chun Zhang, Li-Qun Wu, Yu H. |
| description | Myocardial ischemia, while causing cardiomyocyte injury, can activate innate protective processes, enhancing myocardial tolerance to ischemia. Such processes are present in not only the heart, but also remote organs. In this investigation, we demonstrated a cardioprotective process involving FGF21 from the liver and adipose tissue. In response to myocardial ischemia/reperfusion injury in the mouse, FGF21 was upregulated and released from the hepatic cells and adipocytes into the circulation and interacted with FGFR1 in cardiomyocytes under the mediation of the cell membrane protein β-Klotho, inducing FGFR1 phosphorylation. This action caused phosphorylation of the signaling molecules PI3K p85, Akt1 and BAD, thereby reducing caspase 3 activity, cell death and myocardial infarction in association with improvement of myocardial function. These observations suggest that FGF21 is upregulated and released from the liver and adipose tissue in myocardial injury, contributing to myocardial protection by the mediation of the FGFR1/β-Klotho–PI3K–Akt1–BAD signaling network. |
| doi_str_mv | 10.1038/srep02767 |
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Such processes are present in not only the heart, but also remote organs. In this investigation, we demonstrated a cardioprotective process involving FGF21 from the liver and adipose tissue. In response to myocardial ischemia/reperfusion injury in the mouse, FGF21 was upregulated and released from the hepatic cells and adipocytes into the circulation and interacted with FGFR1 in cardiomyocytes under the mediation of the cell membrane protein β-Klotho, inducing FGFR1 phosphorylation. This action caused phosphorylation of the signaling molecules PI3K p85, Akt1 and BAD, thereby reducing caspase 3 activity, cell death and myocardial infarction in association with improvement of myocardial function. These observations suggest that FGF21 is upregulated and released from the liver and adipose tissue in myocardial injury, contributing to myocardial protection by the mediation of the FGFR1/β-Klotho–PI3K–Akt1–BAD signaling network.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep02767</identifier><identifier>PMID: 24067542</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 631/337 ; 631/443 ; 631/553 ; 631/80 ; Adipocytes ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Adipose Tissue - physiopathology ; AKT1 protein ; Animals ; bcl-Associated Death Protein - metabolism ; Cardiomyocytes ; Cardiotonic Agents - metabolism ; Caspase ; Caspase 3 - metabolism ; Caspase-3 ; Cell death ; Endocrine System - metabolism ; Endocrine System - pathology ; Fibroblast growth factor receptor 1 ; Fibroblast Growth Factors - metabolism ; Gene Silencing ; Glucuronidase ; Heart Function Tests ; Heart Ventricles - metabolism ; Heart Ventricles - pathology ; Heart Ventricles - physiopathology ; Hemodynamics ; Humanities and Social Sciences ; Ischemia ; Klotho protein ; Liver ; Liver - metabolism ; Liver - pathology ; Liver - physiopathology ; Membrane proteins ; Mice ; multidisciplinary ; Myocardial infarction ; Myocardial ischemia ; Myocardial Ischemia - enzymology ; Myocardial Ischemia - pathology ; Myocardial Ischemia - physiopathology ; Myocardial Ischemia - prevention & control ; Myocardial Reperfusion Injury - enzymology ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - physiopathology ; Myocardium ; Myocytes, Cardiac - enzymology ; Myocytes, Cardiac - pathology ; Phosphatidylinositol 3-Kinases ; Phosphorylation ; Protein Binding ; Proto-Oncogene Proteins c-akt - metabolism ; Receptor, Fibroblast Growth Factor, Type 1 - metabolism ; Reperfusion ; RNA, Small Interfering - metabolism ; Rodents ; Science ; Signal Transduction ; Up-Regulation</subject><ispartof>Scientific reports, 2013-09, Vol.3 (1), p.2767-2767, Article 2767</ispartof><rights>The Author(s) 2013</rights><rights>Copyright Nature Publishing Group Sep 2013</rights><rights>Copyright © 2013, Macmillan Publishers Limited. All rights reserved 2013 Macmillan Publishers Limited. All rights reserved</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-5519e7a3b30098fa5a8f97f8c3261f376915f3dd6ecc125f50e1d22498c76d633</citedby><cites>FETCH-LOGICAL-c504t-5519e7a3b30098fa5a8f97f8c3261f376915f3dd6ecc125f50e1d22498c76d633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1897446206/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1897446206?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,25734,27905,27906,36993,36994,44571,53772,53774,74875</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24067542$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Shu Q.</creatorcontrib><creatorcontrib>Roberts, Derek</creatorcontrib><creatorcontrib>Kharitonenkov, Alexei</creatorcontrib><creatorcontrib>Zhang, Brian</creatorcontrib><creatorcontrib>Hanson, Samuel M.</creatorcontrib><creatorcontrib>Li, Yan Chun</creatorcontrib><creatorcontrib>Zhang, Li-Qun</creatorcontrib><creatorcontrib>Wu, Yu H.</creatorcontrib><title>Endocrine Protection of Ischemic Myocardium by FGF21 from the Liver and Adipose Tissue</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Myocardial ischemia, while causing cardiomyocyte injury, can activate innate protective processes, enhancing myocardial tolerance to ischemia. Such processes are present in not only the heart, but also remote organs. In this investigation, we demonstrated a cardioprotective process involving FGF21 from the liver and adipose tissue. In response to myocardial ischemia/reperfusion injury in the mouse, FGF21 was upregulated and released from the hepatic cells and adipocytes into the circulation and interacted with FGFR1 in cardiomyocytes under the mediation of the cell membrane protein β-Klotho, inducing FGFR1 phosphorylation. This action caused phosphorylation of the signaling molecules PI3K p85, Akt1 and BAD, thereby reducing caspase 3 activity, cell death and myocardial infarction in association with improvement of myocardial function. These observations suggest that FGF21 is upregulated and released from the liver and adipose tissue in myocardial injury, contributing to myocardial protection by the mediation of the FGFR1/β-Klotho–PI3K–Akt1–BAD signaling network.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>631/337</subject><subject>631/443</subject><subject>631/553</subject><subject>631/80</subject><subject>Adipocytes</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>Adipose Tissue - physiopathology</subject><subject>AKT1 protein</subject><subject>Animals</subject><subject>bcl-Associated Death Protein - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cardiotonic Agents - metabolism</subject><subject>Caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell death</subject><subject>Endocrine System - metabolism</subject><subject>Endocrine System - pathology</subject><subject>Fibroblast growth factor receptor 1</subject><subject>Fibroblast Growth Factors - metabolism</subject><subject>Gene Silencing</subject><subject>Glucuronidase</subject><subject>Heart Function Tests</subject><subject>Heart Ventricles - metabolism</subject><subject>Heart Ventricles - pathology</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hemodynamics</subject><subject>Humanities and Social Sciences</subject><subject>Ischemia</subject><subject>Klotho protein</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver - physiopathology</subject><subject>Membrane proteins</subject><subject>Mice</subject><subject>multidisciplinary</subject><subject>Myocardial infarction</subject><subject>Myocardial ischemia</subject><subject>Myocardial Ischemia - enzymology</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Ischemia - prevention & control</subject><subject>Myocardial Reperfusion Injury - enzymology</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardium</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Phosphatidylinositol 3-Kinases</subject><subject>Phosphorylation</subject><subject>Protein Binding</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptor, Fibroblast Growth Factor, Type 1 - metabolism</subject><subject>Reperfusion</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Rodents</subject><subject>Science</subject><subject>Signal Transduction</subject><subject>Up-Regulation</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNplkV9rVDEQxYMottQ--AUk4IsKq_mf3BehlG4trNiH1teQTSbdlL3Jmtxb2G_vtdsuq87LDMyPM2c4CL2l5DMl3HxpFTaEaaVfoGNGhJwxztjLg_kInbZ2T6aSrBO0e42OmCBKS8GO0c-LHIqvKQO-rmUAP6SScYn4qvkV9Mnj79viXQ1p7PFyi-eXc0ZxrKXHwwrwIj1AxS4HfBbSpjTAN6m1Ed6gV9GtG5w-9RN0O7-4Of82W_y4vDo_W8y8JGKYSUk70I4vOSGdiU46EzsdjedM0ci16qiMPAQF3lMmoyRAA2OiM16roDg_QV93uptx2UPwkIfq1nZTU-_q1haX7N-bnFb2rjxYrg03hk0CH54Eavk1Qhtsn5qH9dplKGOzVHAtDVGPt97_g96XsebpPUtNp4VQjKiJ-rijfC1tyibuzVBi_wRm94FN7LtD93vyOZ4J-LQD2rTKd1APTv6n9hvgNZ4V</recordid><startdate>20130926</startdate><enddate>20130926</enddate><creator>Liu, Shu Q.</creator><creator>Roberts, Derek</creator><creator>Kharitonenkov, Alexei</creator><creator>Zhang, Brian</creator><creator>Hanson, Samuel M.</creator><creator>Li, Yan Chun</creator><creator>Zhang, Li-Qun</creator><creator>Wu, Yu H.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130926</creationdate><title>Endocrine Protection of Ischemic Myocardium by FGF21 from the Liver and Adipose Tissue</title><author>Liu, Shu Q. ; Roberts, Derek ; Kharitonenkov, Alexei ; Zhang, Brian ; Hanson, Samuel M. ; Li, Yan Chun ; Zhang, Li-Qun ; Wu, Yu H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-5519e7a3b30098fa5a8f97f8c3261f376915f3dd6ecc125f50e1d22498c76d633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>631/337</topic><topic>631/443</topic><topic>631/553</topic><topic>631/80</topic><topic>Adipocytes</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - pathology</topic><topic>Adipose Tissue - physiopathology</topic><topic>AKT1 protein</topic><topic>Animals</topic><topic>bcl-Associated Death Protein - metabolism</topic><topic>Cardiomyocytes</topic><topic>Cardiotonic Agents - metabolism</topic><topic>Caspase</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Cell death</topic><topic>Endocrine System - metabolism</topic><topic>Endocrine System - pathology</topic><topic>Fibroblast growth factor receptor 1</topic><topic>Fibroblast Growth Factors - metabolism</topic><topic>Gene Silencing</topic><topic>Glucuronidase</topic><topic>Heart Function Tests</topic><topic>Heart Ventricles - metabolism</topic><topic>Heart Ventricles - pathology</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hemodynamics</topic><topic>Humanities and Social Sciences</topic><topic>Ischemia</topic><topic>Klotho protein</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver - physiopathology</topic><topic>Membrane proteins</topic><topic>Mice</topic><topic>multidisciplinary</topic><topic>Myocardial infarction</topic><topic>Myocardial ischemia</topic><topic>Myocardial Ischemia - enzymology</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardial Ischemia - prevention & control</topic><topic>Myocardial Reperfusion Injury - enzymology</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Myocardium</topic><topic>Myocytes, Cardiac - enzymology</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Phosphatidylinositol 3-Kinases</topic><topic>Phosphorylation</topic><topic>Protein Binding</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptor, Fibroblast Growth Factor, Type 1 - metabolism</topic><topic>Reperfusion</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Rodents</topic><topic>Science</topic><topic>Signal Transduction</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shu Q.</creatorcontrib><creatorcontrib>Roberts, Derek</creatorcontrib><creatorcontrib>Kharitonenkov, Alexei</creatorcontrib><creatorcontrib>Zhang, Brian</creatorcontrib><creatorcontrib>Hanson, Samuel M.</creatorcontrib><creatorcontrib>Li, Yan Chun</creatorcontrib><creatorcontrib>Zhang, Li-Qun</creatorcontrib><creatorcontrib>Wu, Yu H.</creatorcontrib><collection>SpringerOpen</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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 One Sustainability</collection><collection>ProQuest Central</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Publicly Available Content (ProQuest)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Shu Q.</au><au>Roberts, Derek</au><au>Kharitonenkov, Alexei</au><au>Zhang, Brian</au><au>Hanson, Samuel M.</au><au>Li, Yan Chun</au><au>Zhang, Li-Qun</au><au>Wu, Yu H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endocrine Protection of Ischemic Myocardium by FGF21 from the Liver and Adipose Tissue</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2013-09-26</date><risdate>2013</risdate><volume>3</volume><issue>1</issue><spage>2767</spage><epage>2767</epage><pages>2767-2767</pages><artnum>2767</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Myocardial ischemia, while causing cardiomyocyte injury, can activate innate protective processes, enhancing myocardial tolerance to ischemia. Such processes are present in not only the heart, but also remote organs. In this investigation, we demonstrated a cardioprotective process involving FGF21 from the liver and adipose tissue. In response to myocardial ischemia/reperfusion injury in the mouse, FGF21 was upregulated and released from the hepatic cells and adipocytes into the circulation and interacted with FGFR1 in cardiomyocytes under the mediation of the cell membrane protein β-Klotho, inducing FGFR1 phosphorylation. This action caused phosphorylation of the signaling molecules PI3K p85, Akt1 and BAD, thereby reducing caspase 3 activity, cell death and myocardial infarction in association with improvement of myocardial function. These observations suggest that FGF21 is upregulated and released from the liver and adipose tissue in myocardial injury, contributing to myocardial protection by the mediation of the FGFR1/β-Klotho–PI3K–Akt1–BAD signaling network.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24067542</pmid><doi>10.1038/srep02767</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase 631/337 631/443 631/553 631/80 Adipocytes Adipose tissue Adipose Tissue - metabolism Adipose Tissue - pathology Adipose Tissue - physiopathology AKT1 protein Animals bcl-Associated Death Protein - metabolism Cardiomyocytes Cardiotonic Agents - metabolism Caspase Caspase 3 - metabolism Caspase-3 Cell death Endocrine System - metabolism Endocrine System - pathology Fibroblast growth factor receptor 1 Fibroblast Growth Factors - metabolism Gene Silencing Glucuronidase Heart Function Tests Heart Ventricles - metabolism Heart Ventricles - pathology Heart Ventricles - physiopathology Hemodynamics Humanities and Social Sciences Ischemia Klotho protein Liver Liver - metabolism Liver - pathology Liver - physiopathology Membrane proteins Mice multidisciplinary Myocardial infarction Myocardial ischemia Myocardial Ischemia - enzymology Myocardial Ischemia - pathology Myocardial Ischemia - physiopathology Myocardial Ischemia - prevention & control Myocardial Reperfusion Injury - enzymology Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Myocardium Myocytes, Cardiac - enzymology Myocytes, Cardiac - pathology Phosphatidylinositol 3-Kinases Phosphorylation Protein Binding Proto-Oncogene Proteins c-akt - metabolism Receptor, Fibroblast Growth Factor, Type 1 - metabolism Reperfusion RNA, Small Interfering - metabolism Rodents Science Signal Transduction Up-Regulation |
| title | Endocrine Protection of Ischemic Myocardium by FGF21 from the Liver and Adipose Tissue |
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