Cited by 108TGF-β signaling in diseasesLiver physiology and pathologyThyroid Disorders and Treatments

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Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses

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Alonso-Merino, Elvira, Martín Orozco, Rosa, Ruíz-Llorente, Lidia, Martínez-Iglesias, Olaia A., Velasco-Martín, Juan Pedro, Montero-Pedrazuela, Ana, Fanjul-Rodríguez, Luisa, Contreras-Jurado, Constanza, Regadera, Javier, Aranda, Ana·2016·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1506113113PMC PMC4914168

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Abstract

TGF-β, the most potent profibrogenic factor, acts by activating SMAD (mothers against decapentaplegic) transcription factors, which bind to SMAD-binding elements in target genes. Here, we show that the thyroid hormone triiodothyronine (T3), through binding to its nuclear receptors (TRs), is able to antagonize transcriptional activation by TGF-β/SMAD. This antagonism involves reduced phosphorylation of SMADs and a direct interaction of the receptors with SMAD3 and SMAD4 that is independent of T3-mediated transcriptional activity but requires residues in the receptor DNA binding domain. T3 reduces occupancy of SMAD-binding elements in response to TGF-β, reducing histone acetylation and inhibiting transcription. In agreement with this transcriptional cross-talk, T3 is able to antagonize fibrotic processes in vivo. Liver fibrosis induced by carbon tetrachloride is attenuated by thyroid hormone administration to mice, whereas aged TR knockout mice spontaneously accumulate collagen. Furthermore, skin fibrosis induced by bleomycin administration is also reduced by the thyroid hormones. These findings define an important function of the thyroid hormone receptors and suggest TR ligands could have beneficial effects to block the progression of fibrotic diseases.

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1 retracted

RETRACTED ARTICLE: Propylthiouracil prevents cutaneous and pulmonary fibrosis in the reactive oxygen species murine model of systemic sclerosis
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Retracted
Liver fibrosis
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Authors: Alonso-Merino, E., Martín Orozco, R., Ruíz-Llorente, L., Martínez-Iglesias, O. A., Velasco-Martín, J. P., Montero-Pedrazuela, A., Fanjul-Rodríguez, L., Contreras-Jurado, C., Regadera, J., & Aranda, A.
Affiliations: Consejo Superior de Investigaciones Científicas (ES)
Instituto de Investigaciones Biomédicas “Alberto Sols,” Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, 20829 Madrid, Spain;
Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, Universidad Autónoma de Madrid, 20829 Madrid, Spain
Universidad Autónoma de Madrid (ES)
Corresponding author: Aranda, Ana
ORCID: Montero-Pedrazuela, Ana
Regadera, Javier
Aranda, Ana
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2016-05-31
Volume: 113
Issue: 24
Pages: E3451-60
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.1506113113
PMC: PMC4914168
OpenAlex: W2409493994
Cited by: 108
References: 57
Citations by year: 2026: 6 · 2025: 14 · 2024: 21 · 2023: 10 · 2022: 9 · 2021: 11 · 2020: 10 · 2019: 13 · 2018: 6 · 2017: 4 · 2016: 3
FWCI: 4.51
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.pnas.org/preview_site/misc/userlicense.xhtml (vor, 183 d)
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
Tesis Doctorals en Xarxa (Consorci de Serveis Universitaris de Catalunya) (publishedVersion)
DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Hispana (submittedVersion, other-oa)
Biblos-e Archivo (Universidad Autónoma de Madrid) (submittedVersion, public-domain)
Funders: Ministerio de Economía y Competitividad (BFU2011-28058, BFU2014-53610P)
Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (RD12/0036/0030)
Comunidad de Madrid (S2011/BMD-2328)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
Keywords: thyroid hormones, triiodothyronine, TGF-beta signaling, Smad3, SMAD4, thyroid hormone receptor, transcriptional crosstalk, Smad phosphorylation, Smad binding element, histone acetylation, liver fibrosis, carbon tetrachloride, skin fibrosis, bleomycin, collagen deposition, fibrosis
MeSH terms: Animals, Bleomycin, Carbon Tetrachloride Poisoning, Liver Cirrhosis, Triiodothyronine, Signal Transduction, Transforming Growth Factor beta, Mice, Knockout, Mice, Smad3 Protein, Smad4 Protein

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Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses

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