Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses
Open accessAbstract
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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Thyroid hormones reduce hepatic steatosis by stimulating hepatic lipophagy and mitochondrial biogenesis, and by inhibiting hepatic lipogenesis.
“Thyroid hormones reduce hepatic steatosis by stimulating hepatic lipophagy and mitochondrial biogenesis, and by inhibiting hepatic lipogenesis.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [348]
The introduction links impaired hepatic thyroid action with nonalcoholic fatty liver disease, and reference 30 cites a rat study in which T3 inhibited or reversed fatty liver. But this paper does not state that thyroid hormones reduce steatosis through lipophagy, mitochondrial biogenesis, or inhibition of lipogenesis; its findings concern TGF-β signaling and fibrosis. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThyroid hormones can interfere with fibrogenesis by inhibiting TGFb signalling.
“They can also interfere with fi brogenesis by inhibiting TGFb signalling.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [348]
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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
- 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
- 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 · 2015: 1
- FWCI
- 4.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- 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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