ArticleJournal of cellular and molecular medicine2021
Up-regulation of TβRIII facilitates the osteogenesis of supraspinous ligament-derived fibroblasts from patients with ankylosing spondylitis.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Transforming growth factor-β1 promotes initiation of entheseal pathological bone formation via osteonectin induction in ankylosing spondylitis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Mechanical Strain-Programmed SDC1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Upregulated GDF-15 in Ankylosing Spondylitis: Pathologic Ossification Promotion through Ligament Fibroblast Osteogenic Differentiation.ACR open rheumatology · 2025Article
- Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Sequence of Events in the Pathogenesis of Axial Spondyloarthritis: A Current Review-2023 SPARTAN Meeting Proceedings.Current rheumatology reports · 2024Review
- Down-regulation of long noncoding RNA HULC inhibits the inflammatory response in ankylosing spondylitis by reducing miR-556-5p-mediated YAP1 expression.Journal of orthopaedic surgery and research · 2023Article
- MYC promotes fibroblast osteogenesis by regulating ALP and BMP2 to participate in ectopic ossification of ankylosing spondylitis.Arthritis research & therapy · 2023Article
- Fibroblast Insights into the Pathogenesis of Ankylosing Spondylitis.Journal of inflammation research · 2023Review
- HDAC1 regulates inflammation and osteogenic differentiation of ankylosing spondylitis fibroblasts through the Wnt-Smad signaling pathway.Journal of orthopaedic surgery and research · 2022Article
- Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis.Frontiers in immunology · 2022Review
- Up-regulation of TβRIII facilitates the osteogenesis of supraspinous ligament-derived fibroblasts from patients with ankylosing spondylitis.Journal of cellular and molecular medicine · 2021Article
- Anti-Osteogenic Effect of Danshensu in Ankylosing Spondylitis: AnFrontiers in pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Spinal supraspinous ligament (SL) osteogenesis is the key risk of ankylosing spondylitis (AS), with an unclear pathogenesis. We previously found that transforming growth factor β1 (TGF-β1), bone morphogenetic proteins (eg BMP2) and type III TGF-β1 receptor (TβRIII) expression were markedly up-regulated in AS-SLs. However, the roles of these closely related molecules in AS are unknown. Here, we showed that BMP2, TGF-β1, TβRIII and S100A4 (a fibroblast marker) were abundant in active osteogenic AS-SL tissues. In vitro, AS-SL fibroblasts (AS-SLFs) showed high BMP2, TGF-β1 and TβRIII expression and auto-osteogenic capacity. We further evaluated the role of TβRIII in the osteogenesis of normal SLFs. BMP2 combined with TGF-β1 induced the osteogenesis of TβRIII-overexpressing SLFs, but the activity was lost in SLFs upon TβRIII knockdown. Moreover, our data suggested that BMP2 combined with TGF-β1 significantly activated both TGF-β1/Smad signalling and BMP2/Smad/RUNX2 signalling to induce osteogenesis of SLFs with TβRIII up-regulation. Furthermore, our multi-strategy molecular interaction analysis approach indicated that TGF-β1 presented BMP2 to TβRIII, sequentially facilitating BMP2 recognition by BMPR1A and promoting the osteogenesis of TβRIII-overexpressing SLFs. Collectively, our results indicate that TGF-β1 combined with BMP2 may participate in the osteogenic differentiation of AS-SLF by acting on up-regulated TβRIII, resulting in excessive activation of both TGF-β1/Smad and BMP2/BMPR1A/Smad/RUNX2 signalling.
Indexed as
Identifiers
What OpenQuestion holds
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.