ReviewCell proliferation2024
Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.
Review in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Activation of SLIT2/ROBO1/LRP6 axis aggravates cartilage degradation via β-catenin signaling in TMJOA.JCI insight · 2026Article
- Molecular Mechanisms of Chondrocyte Hypertrophy Mediated by Physical Cues and Therapeutic Strategies in Osteoarthritis.International journal of molecular sciences · 2026Review
- Role of Notch signaling pathway in joint homeostasis and osteoarthritis.Frontiers in bioengineering and biotechnology · 2026Review
- Stromal Vascular Fraction Gel for Osteoarthritis: Mechanisms and Therapeutic Benefits.Stem cells international · 2026Review
- Exploring immune modulation in osteoarthritis: identifying key biomarkers and the role of PTPRC in regulating immune microenvironment for therapeutic intervention.Frontiers in immunology · 2026Article
- Non-viral gene delivery systems for osteoarthritis therapy.Biomaterials translational · 2026Review
- Exosomes Extracted from Human Umbilical Cord MSCs Contribute to Osteoarthritic Cartilage and Chondrocytes Repair Through Enhancing Autophagy While Suppressing the Wnt/β-Catenin Pathway.Tissue engineering and regenerative medicine · 2025Article
- Article
- Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review.Bone research · 2025Review
- Primary cilia and inflammatory response: unveiling new mechanisms in osteoarthritis progression.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Abdominal obesity and osteoarthritis risk: evaluating the association of lipid accumulation product, body roundness index, and waist triglyceride index with osteoarthritis in U.S. adults.Frontiers in nutrition · 2025Article
- CRNDE, a Potential Therapeutic Target in Human Diseases.Current pharmaceutical design · 2025Review
- The multifaceted roles of E3 ubiquitin ligases in osteoarthritis.Frontiers in cell and developmental biology · 2025Review
- Association between TGF-β1 and β-catenin expression in the vaginal wall of patients with pelvic organ prolapse.Open life sciences · 2025Article
- Exosomes in cartilage microenvironment regulation and cartilage repair.Frontiers in cell and developmental biology · 2025Review
- Implications of mechanosensitive ion channels in the pathogenesis of osteoarthritis: a comprehensive review.Frontiers in cell and developmental biology · 2025Review
- Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.Cell proliferation · 2024Review
- The Role of Alarmins in the Pathogenesis of Rheumatoid Arthritis, Osteoarthritis, and Psoriasis.Current issues in molecular biology · 2024Review
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.
Funding
Abstract
Osteoarthritis (OA) is the most prevalent disorder of synovial joint affecting multiple joints. In the past decade, we have witnessed conceptual switch of OA pathogenesis from a 'wear and tear' disease to a disease affecting entire joint. Extensive studies have been conducted to understand the underlying mechanisms of OA using genetic mouse models and ex vivo joint tissues derived from individuals with OA. These studies revealed that multiple signalling pathways are involved in OA development, including the canonical Wnt/β-catenin signalling and its interaction with other signalling pathways, such as transforming growth factor β (TGF-β), bone morphogenic protein (BMP), Indian Hedgehog (Ihh), nuclear factor κB (NF-κB), fibroblast growth factor (FGF), and Notch. The identification of signalling interaction and underlying mechanisms are currently underway and the specific molecule(s) and key signalling pathway(s) playing a decisive role in OA development need to be evaluated. This review will focus on recent progresses in understanding of the critical role of Wnt/β-catenin signalling in OA pathogenesis and interaction of β-catenin with other pathways, such as TGF-β, BMP, Notch, Ihh, NF-κB, and FGF. Understanding of these novel insights into the interaction of β-catenin with other pathways and its integration into a complex gene regulatory network during OA development will help us identify the key signalling pathway of OA pathogenesis leading to the discovery of novel therapeutic strategies for OA intervention.
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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.