ArticleScientific reports2016
Context-specific protection of TGFα null mice from osteoarthritis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.
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
19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- Pooled it
- A Genome-Wide Association Study Meta-Analysis of Alpha Angle Suggests Cam-Type Morphology May Be a Specific Feature of Hip Osteoarthritis in Older Adults.Arthritis & rheumatology (Hoboken, N.J.) · 2023Pooled it
- Genome-wide analyses using UK Biobank data provide insights into the genetic architecture of osteoarthritis.Nature genetics · 2018Pooled it
- Acute TGFα drives OA-associated transcriptional and metabolic remodelling in primary chondrocytes.Osteoarthritis and cartilage open · 2026Article
- PIEZO1 variants that reduce open channel probability are associated with familial osteoarthritis.The Journal of biological chemistry · 2026Article
- Revolutionizing the treatment of intervertebral disc degeneration: an approach based on molecular typing.Journal of translational medicine · 2025Article
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.bioRxiv : the preprint server for biology · 2024Article
- Article
- Advanced nanoparticles in osteoarthritis treatment.Biomaterials translational · 2024Review
- Anabolic phenotype in cartilage-specific mitogen-inducible gene-6 knockout mice is independent of transforming growth factor-α.Osteoarthritis and cartilage open · 2023Article
- Regulation of osteoarthritis development by ADAM17/Tace in articular cartilage.Journal of bone and mineral metabolism · 2022Article
- Understanding cartilage protection in OA and injury: a spectrum of possibilities.BMC musculoskeletal disorders · 2020Review
- Overexpression of MIG-6 in the cartilage induces an osteoarthritis-like phenotype in mice.Arthritis research & therapy · 2020Article
- EGFR Signaling: Friend or Foe for Cartilage?JBMR plus · 2019Review
- Does Joint Injury Make Young Joints Old?The Journal of the American Academy of Orthopaedic Surgeons · 2018Article
- A Pathophysiological Validation of Collagenase II-Induced Biochemical Osteoarthritis Animal Model in Rabbit.Tissue engineering and regenerative medicine · 2018Article
- Gefitinib for Epidermal Growth Factor Receptor Activated Osteoarthritis Subpopulation Treatment.EBioMedicine · 2018Article
- Models to define the stages of articular cartilage degradation in osteoarthritis development.International journal of experimental pathology · 2017Review
- Recent developments in emerging therapeutic targets of osteoarthritis.Current opinion in rheumatology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor alpha (TGFα) is a growth factor involved in osteoarthritis (OA). TGFα induces an OA-like phenotype in articular chondrocytes, by inhibiting matrix synthesis and promoting catabolic factor expression. To better understand TGFα's potential as a therapeutic target, we employed two in vivo OA models: (1) post-traumatic and (2) aging related OA. Ten-week old and six-month old male Tgfa null mice and their heterozygous (control) littermates underwent destabilization of the medial meniscus (DMM) surgery. Disease progression was assessed histologically using the Osteoarthritis Research Society International (OARSI) scoring system. As well, spontaneous disease progression was analyzed in eighteen-month-old Tgfa null and heterozygous mice. Ten-week old Tgfa null mice were protected from OA progression at both seven and fourteen weeks post-surgery. No protection was seen however in six-month old null mice after DMM surgery, and no differences were observed between genotypes in the aging model. Thus, young Tgfa null mice are protected from OA progression in the DMM model, while older mice are not. In addition, Tgfa null mice are equally susceptible to spontaneous OA development during aging. Thus, TGFα might be a valuable therapeutic target in some post-traumatic forms of OA, however its role in idiopathic disease is less clear.
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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.