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. 2018 Oct 23;8:15642. doi: 10.1038/s41598-018-33958-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

The role of electrical remodeling of TBX5 insufficiency in atrial fibrillation. (a) The schematic illustration of the impact of TBX5 loss-of-function mutation on ionic currents/action potential duration (APD). TBX5-deletion leads to reductions in I_Na, I_to, I_Kur, I_K1, SERCA and RyR. Reduced repolarizing potassium currents (e.g., I_to and I_Kur) lead to prolonged APD. Suppression of I_K1 and increased I_NCX due to cytosolic calcium overload lead to phase 4 depolarization and predispose to spontaneous depolarizations. (b) TBX5 regulates PITX2 expression, and TBX5 and PITX2 antagonistically regulate downstream targets. Reduced PITX2 leads to upregulation of I_Na, I_Ks, SERCA and RyR, and downregulation of I_CaL and I_K1. Loss of TBX5 leads to prolonged APD, whereas loss of PITX2 leads to shortened APD. Therefore, reduced PITX2 in TBX5-mutant atria contributes to a protective mechanism.