ReviewArthritis research & therapy2016
Smad-dependent mechanisms of inflammatory bone destruction.
Review in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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
29 citing papers in PubMed, 51 citations in OpenAlex.
- Temporarily increased TGFβ following radon spa correlates with reduced pain while serum IL-18 is a general predictive marker for pain sensitivity.Radiation and environmental biophysics · 2019Trial
- Network pharmacology, molecular docking, and experimental validation of the mechanisms of Withaferin a in treating periodontitis.Clinical oral investigations · 2026Article
- Cellular crosstalk and signaling networks in the rheumatoid arthritis synovial microenvironment.Journal of translational medicine · 2026Review
- Regulation of immune microenvironments by polyetheretherketone surface topography for improving osseointegration.Journal of nanobiotechnology · 2025Article
- Human Chorionic Gonadotropin Regulates the Smad Signaling Pathway by Antagonizing TGF-β in Giant Cell Tumor of Bone.Recent patents on anti-cancer drug discovery · 2024Article
- Research Progress in Function and Regulation of E3 Ubiquitin Ligase SMURF1.Current medical science · 2023Review
- Review
- Cellular mechanotransduction in health and diseases: from molecular mechanism to therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Towards a Unified Approach in Autoimmune Fibrotic Signalling Pathways.International journal of molecular sciences · 2023Review
- Pharmacological action ofFrontiers in pharmacology · 2023Review
- Comparison of growth performance and related gene expression of muscle and fat from Landrace, Yorkshire, and Duroc and Woori black pigs.Journal of animal science and technology · 2023Article
- The Association of uPA, uPAR, and suPAR System with Inflammation and Joint Damage in Rheumatoid Arthritis: suPAR as a Biomarker in the Light of a Personalized Medicine Perspective.Journal of personalized medicine · 2022Article
- Incidence of Hip Fractures among Patients with Chronic Otitis Media: The Real-World Data.Medicina (Kaunas, Lithuania) · 2022Article
- The Role of Long Non-Coding RNAs in Epithelial-Mesenchymal Transition-Related Signaling Pathways in Prostate Cancer.Frontiers in molecular biosciences · 2022Review
- Genipin modified lyophilized platelet-rich fibrin scaffold for sustained release of growth factors to promote bone regeneration.Frontiers in physiology · 2022Article
- Circular RNAs as potential regulators in bone remodeling: a narrative review.Annals of translational medicine · 2021Review
- Review
- The Smad Dependent TGF-β and BMP Signaling Pathway in Bone Remodeling and Therapies.Frontiers in molecular biosciences · 2021Review
- Influence of the TGF-β Superfamily on Osteoclasts/Osteoblasts Balance in Physiological and Pathological Bone Conditions.International journal of molecular sciences · 2020Review
- MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head.Journal of orthopaedic surgery and research · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homeostatic bone remodelling becomes disturbed in a variety of pathologic conditions that affect the skeleton, including inflammatory diseases. Rheumatoid arthritis is the prototype of an inflammatory arthritis characterised by chronic inflammation, progressive cartilage destruction and focal bone erosions and is a prime example for a disease with disturbed bone homeostasis. The inflammatory milieu favours the recruitment and activation of osteoclasts, which have been found to be the cells that are primarily responsible for bone erosions in many animal models of inflammatory arthritis. Among the inflammatory modulators, members of the transforming growth factor (TGF)-β super family are shown to be important regulators in osteoclastogenesis with Smad-mediated signalling being crucial for inducing osteoclast differentiation. These findings have opened a new field for exploring mechanisms of osteoclast differentiation under inflammatory conditions. Recent studies have shown that the TGF-β superfamily members TGF-β1, myostatin and activin A directly regulate osteoclast differentiation through mechanisms that depend on the RANKL-RANK interplay. These growth factors transduce their signals through type I and II receptor serine/threonine kinases, thereby activating the Smad pathway. In this review, we describe the impact of inflammation-induced Smad signalling in osteoclast development and subsequently bone erosion in rheumatoid arthritis.
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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.