ArticleMolecular metabolism2024
Thyroid hormone receptor beta (THRβ1) is the major regulator of T3 action in human iPSC-derived hepatocytes.
Article in Molecular metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Interorgan Crosstalk in MASLD: A Narrative Review.Biomedicines · 2026Review
- Metabolic and hepatic differences among biochemically euthyroid individuals with distinct thyroid hormone sources: a comparative study.BMC endocrine disorders · 2026Article
- Thyroid hormone acts independently of the thyroid hormone receptor beta in hepatocytes to improve systemic insulin sensitivity.Hepatology communications · 2026Article
- Mechanisms and Prognostic Assessment Value of Thyroid Hormone in Liver Failure.Journal of clinical and translational hepatology · 2026Review
- Repurposing levothyroxine for managing metabolic dysfunction-associated steatotic liver disease.Endocrine · 2025Review
- Chronic Inflammation and Immune Dysregulation in Metabolic-Dysfunction-Associated Steatotic Liver Disease Progression: From Steatosis to Hepatocellular Carcinoma.Biomedicines · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
objectiveThyroid hormone (TH) action is mediated by thyroid hormone receptor (THR) isoforms. While THRβ1 is likely the main isoform expressed in liver, its role in human hepatocytes is not fully understood.
methodsTo elucidate the role of THRβ1 action in human hepatocytes we used CRISPR/Cas9 editing to knock out THRβ1 in induced pluripotent stem cells (iPSC). Following directed differentiation to the hepatic lineage, iPSC-derived hepatocytes were then interrogated to determine the role of THRβ1 in ligand-independent and -dependent functions.
resultsWe found that the loss of THRβ1 promoted alterations in proliferation rate and metabolic pathways regulated by T3, including gluconeogenesis, lipid oxidation, fatty acid synthesis, and fatty acid uptake. We observed that key genes involved in liver metabolism are regulated through both T3 ligand-dependent and -independent THRβ1 signaling mechanisms. Finally, we demonstrate that following THRβ1 knockout, several key metabolic genes remain T3 responsive suggesting they are THRα targets.
conclusionsThese results highlight that iPSC-derived hepatocytes are an effective platform to study mechanisms regulating TH signaling in human hepatocytes.
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