ArticleNature communications2018
Reciprocal inhibition of YAP/TAZ and NF-κB regulates osteoarthritic cartilage degradation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 1 of them a synthesis that pooled it.
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
206 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.
- Rejuvenation of Bone Marrow Mesenchymal Stem Cells: Mechanisms and Their Application in Senile Osteoporosis Treatment.Biomolecules · 2025Pooled it
- Deciphering the function and mechanism of extracorporeal shock wave therapy in knee osteoarthritis (Review).International journal of molecular medicine · 2026Review
- Multi-omics-guided HAMA/PLMA bioink integrating mechanical support, antibacterial protection, and liposomal kartogenin for cartilage regeneration.Materials today. Bio · 2026Article
- Cell differentiation-related signaling pathways: biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Article
- Obesity-Associated Osteoarthritis: Mechanical-Metabolic Pathogenesis, Obesity Memory and Dual-Target Therapy.Current obesity reports · 2026Review
- Early targeting of the YAP/TEAD-PKC-NF-κB axis alleviates post-traumatic osteoarthritis.iScience · 2026Article
- From Joint Loading to Osteoarthritis: A Multiscale Review of Knee Mechanobiology and Digital Modelling.International journal of molecular sciences · 2026Review
- Neuronal and Glial YAP/TAZ in the Spinal Cord Contribute to the Development of Bone Cancer Pain in Mice.Neuroscience bulletin · 2026Article
- A Piezo-Mimetic Ionic Hydrogel Harnessing Joint Motion for Cartilage Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Combination of Three Herbal Components (ISL, Que, Meth) Suppresses Uveal Melanoma Growth via Gαq/MEK/YAP Axis Modulation and Apoptosis.Biomedicines · 2026Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Disruption of YAP biomolecular condensates by mechanical stress drives intervertebral disc vascularization.Science advances · 2026Article
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- Exploring cartilage development and disease models: applications of cartilage organoids.Inflammation and regeneration · 2026Review
- Long non-coding RNA CKMT2-AS1 serves as a biomarker for osteoarthritis and participates in chondrocyte injury via miR-6720-5p.Journal of orthopaedic surgery and research · 2026Article
- YAP1 Knockdown Reduces IL-1β-Induced Human Chondrocyte Inflammation and Promotes Human MSC Chondrogenesis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- 3D-embedding of human gingiva-derived mesenchymal stromal cells in "VitroGelBMC oral health · 2026Article
- Article
- Role of external forces in the mechanobiology of stem and differentiated chondrogenic cells embedded in a tissue-engineered construct for cartilage repair.Journal of biomedical science · 2026Review
146 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis is one of the leading causes of pain and disability in the aged population due to articular cartilage damage. This warrants investigation of signaling mechanisms that could protect cartilage from degeneration and degradation. Here we show in a murine model of experimental osteoarthritis that YAP activation by transgenic overexpression or by deletion of its upstream inhibitory kinases Mst1/2 preserves articular cartilage integrity, whereas deletion of YAP in chondrocytes promotes cartilage disruption. Our work shows that YAP is both necessary and sufficient for the maintenance of cartilage homeostasis in osteoarthritis. Mechanistically, inflammatory cytokines, such as TNFα or IL-1β, trigger YAP/TAZ degradation through TAK1-mediated phosphorylation. Furthermore, YAP directly interacts with TAK1 and attenuates NF-κB signaling by inhibiting substrate accessibility of TAK1. Our study establishes a reciprocal antagonism between Hippo-YAP/TAZ and NF-κB signaling in regulating the induction of matrix-degrading enzyme expression and cartilage degradation during osteoarthritis pathogenesis.
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.