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Our previous study showed that Fe<jats:sup>2+<\/jats:sup> uptake in thalassemic cardiomyocytes are mainly mediated by T\u2010type calcium channels (TTCC). Nevertheless, the role of TTCC as well as other transporters such as divalent metal transporter1 (DMT1) and L\u2010type calcium channels (LTCC) as possible portals for iron entry into the heart in <jats:italic>in vivo<\/jats:italic> thalassemic mice under an iron\u2010overload condition has not been investigated.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> An iron\u2010overload condition was induced in genetically altered \u03b2\u2010thalassemic mice and adult wild\u2010type mice by feeding them with an iron diet (0.2% ferrocene w\/w) for 3\u2003months. Then, blockers for LTCC (verapamil and nifedipine), TTCC (efonidipine), and DMT1 (ebselen) as well as iron chelator desferoxamine (DFO) were given for 1\u2003month with continuous iron feeding.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Treatment with LTCC, TTCC, DMT1 blockers, and DFO reduced cardiac iron deposit, cardiac malondialdehyde (MDA), plasma non\u2010transferrin\u2010bound iron, and improved heart rate variability and left ventricular (LV) function in thalassemic mice with iron overload. Only TTCC and DMT1 blockers and DFO reduced liver iron accumulation, liver MDA, plasma MDA, and decreased mortality rate in iron\u2010overloaded thalassemic mice.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> DMT1, LTCC, and TTCC played important roles for iron entry in the thalassemic heart under an iron\u2010overloaded condition. Unlike LTCC blocker, TTCC blocker provided all benefits including attenuating iron deposit in both the heart and liver, reduced oxidative stress, and decreased mortality in iron\u2010overloaded mice.<\/jats:p>","DOI":"10.1111\/j.1600-0609.2012.01779.x","type":"journal-article","created":{"date-parts":[[2012,3,8]],"date-time":"2012-03-08T08:59:52Z","timestamp":1331197192000},"page":"535-548","source":"Crossref","is-referenced-by-count":94,"title":["T\u2010type calcium channel blockade improves survival and cardiovascular function in thalassemic 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