{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T12:48:33Z","timestamp":1793623713349,"version":"4.5.0"},"reference-count":46,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2015,10,13]],"date-time":"2015-10-13T00:00:00Z","timestamp":1444694400000},"content-version":"vor","delay-in-days":33,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100005010","name":"Associazione Italiana per la Ricerca sul Cancro","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005010","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BioFactors"],"published-print":{"date-parts":[[2015,9,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Transferrin receptor 2 (Tfr2) is an iron\u2010modulator transcribed in two isoforms, Tfr2\u03b1 and Tfr2\u03b2. The latter is expressed in the heart. We obtained two mouse models with silencing of Tfr2\u03b2: one with a normal systemic iron amount (SIA), <jats:italic>i.e.,<\/jats:italic> Tfr2\u2010KI, and the other, <jats:italic>i.e.,<\/jats:italic> LCKO\u2010KI, with high SIA due to hepatic Tfr2\u03b1 silencing. We aimed to assess whether Tfr2\u03b2 might play a role in myocardial injury and whether Tfr2\u03b2 silencing might modify proteins of iron metabolism, antioxidant, apoptotic, and survival enzyme activities in the heart undergoing ischemia\/reperfusion (I\/R).<\/jats:p><jats:p>Isolated hearts of wild\u2010type (WT) and Tfr2\u2010null mice were studied before or after an I\/R protocol, and proteins\/RNA analyzed by Western blot and\/or quantitative PCR.<\/jats:p><jats:p>Tfr2\u03b2 increased in WT hearts subject to I\/R, and both Tfr2\u03b2 null mice hearts were protected against I\/R injury (about 40% smaller infarct\u2010size compared to WT hearts). RISK kinases (ERK1\/2\u2010AKT\u2010PKC\u03b5) were found up\u2010regulated after I\/R in Tfr2\u2010KI, whereas SAFE enzyme (Stat3) and GSK3\u03b2 resulted phosphorylated during I\/R in LCKO\u2010KI hearts. While HO\u20101 and HIF\u20102a were high in both Tfr2\u03b2\u2010null mice, Catalase, and proapoptotic factors were upregulated only in LCKO\u2010KI. Finally, Tfr2\u2010KI hearts presented an increased Ferritin\u2010H and a decreased Ferroportin1, whereas LCKO\u2010KI hearts displayed an upregulation of Ferritin\u2010L chain and DMT1\/Hamp\u2010RNA.<\/jats:p><jats:p>In conclusion, Tfr2\u03b2 isoform is involved in cardiac iron metabolism and its silencing leads to a protected phenotype (antioxidants, RISK, and\/or SAFE upregulation) against I\/R challenging. Iron\u2010dependent signals involved in cardioprotection seem to be positively affected by Tfr2\u03b2 downregulation and subsequent Ferritins upregulation. \u00a9 2015 BioFactors, 41(5):360\u2013371, 2015<\/jats:p>","DOI":"10.1002\/biof.1237","type":"journal-article","created":{"date-parts":[[2017,2,24]],"date-time":"2017-02-24T12:56:52Z","timestamp":1487941012000},"page":"360-371","source":"Crossref","is-referenced-by-count":21,"title":["A comparative study of myocardial molecular phenotypes of two tfr2\u03b2 null mice: Role in ischemia\/reperfusion"],"prefix":"10.1002","volume":"41","author":[{"given":"Martina","family":"Boero","sequence":"first","affiliation":[{"name":"Department of Clinical and Biological Sciences University of Torino AOU San Luigi Gonzaga, Orbassano, Torino Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pasquale","family":"Pagliaro","sequence":"additional","affiliation":[{"name":"Department of Clinical and Biological Sciences University of 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