{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T01:04:06Z","timestamp":1780707846186,"version":"3.54.1"},"reference-count":0,"publisher":"S. Karger AG","issue":"1-2","license":[{"start":{"date-parts":[[2019,9,12]],"date-time":"2019-09-12T00:00:00Z","timestamp":1568246400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2019,9,12]],"date-time":"2019-09-12T00:00:00Z","timestamp":1568246400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pharmacology"],"published-print":{"date-parts":[[2020]]},"abstract":"<b><i>Background and Purpose:<\/i><\/b> Intracellular calcium concentration ([Ca<sup>2+<\/sup>]i) overload occurs in myocardial ischemia and \u00adreperfusion. The augmentation of the late sodium current (I<sub>NaL<\/sub>) causes intracellular Na<sup>+<\/sup> accumulation and subsequent [Ca<sup>2+<\/sup>]i overload via the reverse mode of the Na<sup>+<\/sup>\/Ca<sup>2+<\/sup> exchange current (reverse-I<sub>NCX<\/sub>), which can lead to arrhythmia and cardiac dysfunction. Thus, inhibition of I<sub>NaL<\/sub> is a potential therapeutic approach for ischemic heart disease. The aim of this study was to investigate the effects of thyroid hormone on augmented I<sub>NaL<\/sub>, reverse-I<sub>NCX<\/sub>, altered action potential duration (APD), and [Ca<sup>2+<\/sup>]i concentration in hypoxia\/reoxygenation (H\/R)-induced ventricular myocytes in vitro. <b><i>Methods:<\/i><\/b> The transient Na<sup>+<\/sup> current (I<sub>NaT<\/sub>), I<sub>NaL<\/sub>, reverse-I<sub>NCX<\/sub>, and APs were recorded using a whole-cell patch-clamp technique in neonatal mouse ventricular myocytes. [Ca<sup>2+<\/sup>]i concentration alteration were, respectively, observed by confocal microscopy and flow cytometry. <b><i>Results:<\/i><\/b> Triiodothyronine (T3) pretreatment decreased the I<sub>NaL<\/sub> in a concentration-dependent manner. H\/R injury aggravated the I<sub>NaL<\/sub>, I<sub>NaT<\/sub>, and reverse-I<sub>NCX<\/sub> in cardiomyocytes and increased the continuous accumulation of [Ca<sup>2+<\/sup>]i (<i>p<\/i> &#x3c; 0.05). The application of T3 prior to H\/R injury significantly decreased the increased I<sub>NaL<\/sub>, I<sub>NaT<\/sub>, and reverse-I<sub>NCX<\/sub> and blunted the [Ca<sup>2+<\/sup>]i increase. Furthermore, T3 pretreatment shortened the APD induced by H\/R injury. <b><i>Conclusion:<\/i><\/b> T3 inhibited H\/R-increased I<sub>NaL<\/sub> and reverse I<sub>NCX<\/sub> augmentation, shortened the APD, and diminished [Ca<sup>2+<\/sup>]i overload, indicating a potential therapeutic use of T3 as an I<sub>NaL<\/sub> inhibitor to maintain Ca<sup>2+<\/sup> homeostasis and protect cardiomyocytes against H\/R injury.<\/jats:p>","DOI":"10.1159\/000502804","type":"journal-article","created":{"date-parts":[[2019,9,12]],"date-time":"2019-09-12T21:00:33Z","timestamp":1568322033000},"page":"63-72","source":"Crossref","is-referenced-by-count":11,"title":["Thyroid Hormone Diminishes Ca<sup>2+<\/sup> Overload Induced by Hypoxia\/Reoxygenation in Cardiomyocytes by Inhibiting Late Sodium Current and Reverse-Na<sup>+<\/sup>\/Ca<sup>2+<\/sup> Exchange Current"],"prefix":"10.1159","volume":"105","author":[{"given":"Bin","family":"Zeng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoting","family":"Liao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huaiyu","family":"Ruan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caixia","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2019,9,12]]},"container-title":["Pharmacology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/502804","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/502804","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T15:55:02Z","timestamp":1745423702000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000502804"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2019,9,12]]},"references-count":0,"journal-issue":{"issue":"1-2","published-online":{"date-parts":[[2020,1,22]]},"published-print":{"date-parts":[[2020,1,28]]}},"URL":"https:\/\/doi.org\/10.1159\/000502804","archive":["Portico"],"relation":{},"ISSN":["0031-7012","1423-0313"],"issn-type":[{"value":"0031-7012","type":"print"},{"value":"1423-0313","type":"electronic"}],"subject":[],"published":{"date-parts":[[2019,9,12]]}}}