ArticleExperimental and therapeutic medicine2020
Estrogen downregulates TAK1 expression in human fibroblast-like synoviocytes and in a rheumatoid arthritis model.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Research trends in estrogen and rheumatoid arthritis: a systematic bibliometric approach.Biology of sex differences · 2025Pooled it
- Sex-dependent mechanisms in rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- Absent in melanoma 2 (AIM2) in rheumatoid arthritis: novel molecular insights and implications.Cellular & molecular biology letters · 2022Review
- Yi Shen Juan Bi Pill alleviates bone destruction in inflammatory arthritis under postmenopausal conditions by regulating ephrinB2 signaling.Frontiers in pharmacology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor β-activated kinase-1 (TAK1), a member of the mitogen-activated protein kinase family, plays a key role in the pathogenesis and progression of rheumatoid arthritis (RA). Estrogen has been previously reported to delay arthritis progression. However, the exact association between TAK1 and estrogen remains elusive. The present study demonstrated that TAK1 was upregulated in synoviocytes of patients with RA compared with patients with osteoarthritis and healthy controls. In addition, TAK1 was also expressed in cultured fibroblast-like synoviocytes (FLS), and its levels decreased significantly in 17β-estradiol (E2)-treated cells in a dose-dependent manner. Furthermore, administration of E2 significantly decreased TAK1 expression and attenuated the development of collagen-induced arthritis (CIA). Taken together, the findings of the present study suggested that E2 mediates a decrease of TAK1 in both FLS and CIA, which subsequently results in a suppression of the pathological process of CIA. Therefore, estrogen may serve as a potential therapeutic agent for the treatment of RA by targeting TAK1.
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Registered trials
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