ReviewAnnals of the New York Academy of Sciences2010
Beta-catenin, cartilage, and osteoarthritis.
Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 59 citations in OpenAlex.
- Epigenetic Biomarkers in Temporomandibular Joint Osteoarthritis: An Emerging Target in Treatment.International journal of molecular sciences · 2025Review
- Development of novel osteoarthritis therapy by targeting AMPK-β-catenin-Runx2 signaling.Genes & diseases · 2025Review
- Application of kartogenin for the treatment of cartilage defects: current practice and future directions.RSC advances · 2024Review
- Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.Cell proliferation · 2024Review
- LncRNA-mediated cartilage homeostasis in osteoarthritis: a narrative review.Frontiers in medicine · 2024Review
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- MicroRNAs-mediated regulation pathways in rheumatic diseases.Inflammopharmacology · 2023Review
- The intricate mechanism of PLS3 in bone homeostasis and disease.Frontiers in endocrinology · 2023Review
- Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression.Frontiers in immunology · 2023Review
- Plastin 3 in health and disease: a matter of balance.Cellular and molecular life sciences : CMLS · 2021Review
- Circ_0116061 regulated the proliferation, apoptosis, and inflammation of osteoarthritis chondrocytes through regulating the miR-200b-3p/SMURF2 axis.Journal of orthopaedic surgery and research · 2021Article
- Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase Promotes Inflammation and Accelerates Osteoarthritis by Activating β-Catenin.Frontiers in cell and developmental biology · 2021Article
- Runx2 plays a central role in Osteoarthritis development.Journal of orthopaedic translation · 2020Review
- Association between sleep duration and osteoarthritis and their prevalence in Koreans: A cross-sectional study.PloS one · 2020Article
- Epigenetic and therapeutic implications of dnmt3b in temporomandibular joint osteoarthritis.American journal of translational research · 2019Article
- Effects of Qi-Fang-Xi-Bi-Granules on Cartilage Morphology and C/ebpEvidence-based complementary and alternative medicine : eCAM · 2018Article
- Wnt/β-catenin Signaling in Osteoarthritis and in Other Forms of Arthritis.Current rheumatology reports · 2017Review
- Leukocyte Cell-Derived Chemotaxin-2: It's Role in Pathophysiology and Future in Clinical Medicine.Clinical and translational science · 2017Review
- Loss of spatial organization and destruction of the pericellular matrix in early osteoarthritis in vivo and in a novel in vitro methodology.Osteoarthritis and cartilage · 2016Article
- A Qualitative Model of the Differentiation Network in Chondrocyte Maturation: A Holistic View of Chondrocyte Hypertrophy.PloS one · 2016Article
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
The early cellular events during the development of osteoarthritis (OA) are accelerated articular chondrocyte maturation and extracellular matrix degradation, which are usually seen in the weight-bearing region of articular cartilage. The results of our recent studies from transgenic OA mouse models indicate that upregulation of beta-catenin signaling in articular chondrocytes is most likely responsible for the conversion of normal articular chondrocytes into maturing (arthritic) chondrocytes, which is associated with activation of chondrocyte maturational genes and matrix degradation. Conditional activation of the beta-catenin gene in articular chondrocytes leads to an OA-like phenotype. Overexpression of Smurf2, an E3 ubiquitin ligase, also induces an OA-like phenotype through upregulation of beta-catenin signaling. In addition, beta-catenin upregulation was also found in articular cartilage tissues in patients with OA. These findings indicate that beta-catenin plays a central role in articular cartilage function and that activation of beta-catenin signaling may represent a pathologic mechanism for OA development.
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.