ArticleEndocrine2012
Thalidomide inhibits adipogenesis of orbital fibroblasts in Graves' ophthalmopathy.
Article in Endocrine, 2012. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Stimulation of Piezo1 Mechanosensitive Channels Inhibits Adipogenesis in Thyroid Eye Disease.The Journal of clinical endocrinology and metabolism · 2025Article
- Novel perspectives on the pharmacological treatment of thyroid-associated ophthalmopathy.Frontiers in endocrinology · 2024Review
- PPAR agonists attenuate lenalidomide's anti-myeloma activity in vitro and in vivo.Cancer letters · 2022Article
- PD-L1 Inhibits T Cell-Induced Cytokines and Hyaluronan ExpressionFrontiers in immunology · 2022Article
- Mechanism of immunomodulatory drugs' action in the treatment of multiple myeloma.Acta biochimica et biophysica Sinica · 2014Review
- Treating Graves' orbitopathy: where are we?Endocrine · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expansion of orbital adipose tissue is a main pathophysiology of Graves' ophthalmopathy (GO), which is an inflammatory autoimmune disease in the orbital region. The effects of immunosuppressive drugs on adipogenesis of orbital fibroblasts have not been determined. Thalidomide, as an immunosuppressive drug, has recently been used in the therapy of many autoimmune diseases. In this study, we analyzed the effects of thalidomide on adipogenesis and found that adipocyte differentiation from preadipocytes in the orbital region was enhanced, which was demonstrated by enhanced expression of peroxisome proliferator activated receptor γ (PPARγ), ap2, and thyroid-stimulating hormone receptor (TSHR). The expression of inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 6 (IL-6) was also increased in GO. Thalidomide dose-dependently inhibited adipogenesis of 3T3-L1 preadipocytes and orbital fibroblasts from GO patients. Along with the inhibited adipogenesis, the expression of TSHR, TNFα, and IL-6 was also down-regulated. We discovered that the mechanism for thalidomide inhibiting adipogenesis was the down-regulation of PPARγ, rather than C/EBPβ and C/EBPδ. We suggest that, besides its canonical anti-TNFα effect, thalidomide plays a role in inhibiting adipogenesis of orbital fibroblasts in GO patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.