Deciphering the roles of triiodothyronine (T3) and thyroid stimulating hormone (TSH) on cardiac electrical remodeling in clinical and experimental hypothyroidism
dc.contributor.author | Casis Sáenz, Oscar | |
dc.contributor.author | Echeazarra, Leyre | |
dc.contributor.author | Sáenz Díez, Beatriz | |
dc.contributor.author | Gallego Muñoz, Mónica | |
dc.date.accessioned | 2024-02-08T10:16:29Z | |
dc.date.available | 2024-02-08T10:16:29Z | |
dc.date.issued | 2024-02 | |
dc.identifier.citation | Journal of Physiology and Biochemistry 809(1) : 1-9 (2024) | es_ES |
dc.identifier.issn | 1138-7548 | |
dc.identifier.uri | http://hdl.handle.net/10810/65224 | |
dc.description.abstract | Hypothyroidism is the most frequent endocrine pathology. Although clinical or overt hypothyroidism has been traditionally associated to low T3 / T4 and high thyrotropin (TSH) circulating levels, other forms exist such as subclinical hypothyroidism, characterized by normal blood T3 / T4 and high TSH. In its different forms is estimated to affect approximately 10% of the population, especially women, in a 5:1 ratio with respect to men. Among its consequences are alterations in cardiac electrical activity, especially in the repolarization phase, which is accompanied by an increased susceptibility to cardiac arrhythmias. Although these alterations have traditionally been attributed to thyroid hormone deficiency, recent studies, both clinical trials and experimental models, demonstrate a fundamental role of TSH in cardiac electrical remodeling. Thus, both metabolic thyroid hormones and TSH regulate cardiac ion channel expression in many and varied ways. This means that the different combinations of hormones that predominate in different types of hypothyroidism (overt, subclinic, primary, central) can generate different forms of cardiac electrical remodeling. These new findings are raising the relevant question of whether serum TSH reference ranges should be redefined. | es_ES |
dc.description.sponsorship | Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature. The work has been financed by the Basque Government (IT1707-22) and the Ministerio de Ciencia e Innovación, MICINN (PID2020-118814RB-I00). BS-D is a predoctoral fellow of the UPV/EHU (PIF21/313). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Springer | es_ES |
dc.relation | info:eu-repo/grantAgreement/MICINN/PID2020-118814RB-I00 | |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | arrhythmia | es_ES |
dc.subject | cardiac electrophysiology | |
dc.subject | electrical remodeling | |
dc.subject | endocrine disease | |
dc.title | Deciphering the roles of triiodothyronine (T3) and thyroid stimulating hormone (TSH) on cardiac electrical remodeling in clinical and experimental hypothyroidism | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.rights.holder | 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. | * |
dc.relation.publisherversion | https://link.springer.com/article/10.1007/s13105-023-01000-z | |
dc.identifier.doi | 10.1007/s13105-023-01000-z | |
dc.departamentoes | Fisiología | es_ES |
dc.departamentoeu | Fisiologia | es_ES |
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