ArticlePLoS biology2019
Up-regulation of FOXD1 by YAP alleviates senescence and osteoarthritis.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 161 citations in OpenAlex.
- Research progress of mesenchymal stem cells/stromal cells and their derivatives against cell senescence in the treatment of osteoarthritis.Annals of medicine · 2026Review
- Early targeting of the YAP/TEAD-PKC-NF-κB axis alleviates post-traumatic osteoarthritis.iScience · 2026Article
- Disruption of YAP biomolecular condensates by mechanical stress drives intervertebral disc vascularization.Science advances · 2026Article
- Exploring molecular signatures of senescence with marker, an R Toolkit for evaluating gene sets as phenotypic markers.NAR genomics and bioinformatics · 2026Article
- YAP1 Upregulates Cytoskeleton Regulator ARHGEF1 and Tissue Regeneration Factor NEDD9 in a Multiplex Proteomic Study.Neurology international · 2026Article
- Mechanosensor YAP orchestrates human neural rosette morphogenesis via TEAD4-LEF1 transcriptional nexus.Science China. Life sciences · 2026Article
- Notch-1 induces M2 polarization of tumor-associated macrophages via the YAP/EZH2/FOXD1/CD47 signaling axis, thereby driving non-small cell lung cancer progression.Frontiers in medicine · 2026Article
- Mechanism driven adaptation of smart hydrogels to the osteoarthritis pathological microenvironment.Frontiers in bioengineering and biotechnology · 2026Review
- Signaling pathways and ion channels in osteoarthritis: a review of recent advances.Frontiers in immunology · 2026Review
- Exosomal miRNA-25-3p from platelet-rich plasma alleviates chondrocyte pyroptosis and knee osteoarthritis by regulating MAP4K2/Hippo/TNFAIP3 pathway.Functional & integrative genomics · 2025Article
- Molecular signaling pathways in osteoarthritis and biomaterials for cartilage regeneration: a review.Bioengineered · 2025Review
- Association of macrophage colony-stimulating factor 1 and its locus with osteoarthritis: Mendelian randomization and colocalization analysis.Clinical rheumatology · 2025Article
- Recent advances in CAR-MSCs: the new engine of cellular immunotherapy evolution.Journal of hematology & oncology · 2025Review
- Aging microenvironment in osteoarthritis focusing on early-stage alterations and targeted therapies.Bone research · 2025Review
- The Hippo signaling pathway as a therapeutic target in Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Cellular senescence and other age-related mechanisms in skeletal diseases.Bone research · 2025Review
- Aging-dependent YAP1 reduction contributes to AD pathology by upregulating the Nr4a1-AKT/GSK-3β axis.Translational neurodegeneration · 2025Article
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- Targeting PIK3CB/YAP1 improves the sensitivity of paclitaxel by suppressing aging in head and neck squamous tumor cells.Cancer cell international · 2025Article
- FOXM1 expression reverts aging chromatin profiles through repression of the senescence-associated pioneer factor AP-1.Nature communications · 2025Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a driver of various aging-associated disorders, including osteoarthritis. Here, we identified a critical role for Yes-associated protein (YAP), a major effector of Hippo signaling, in maintaining a younger state of human mesenchymal stem cells (hMSCs) and ameliorating osteoarthritis in mice. Clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR associated protein 9 nuclease (Cas9)-mediated knockout (KO) of YAP in hMSCs resulted in premature cellular senescence. Mechanistically, YAP cooperated with TEA domain transcriptional factor (TEAD) to activate the expression of forkhead box D1 (FOXD1), a geroprotective protein. YAP deficiency led to the down-regulation of FOXD1. In turn, overexpression of YAP or FOXD1 rejuvenated aged hMSCs. Moreover, intra-articular administration of lentiviral vector encoding YAP or FOXD1 attenuated the development of osteoarthritis in mice. Collectively, our findings reveal YAP-FOXD1, a novel aging-associated regulatory axis, as a potential target for gene therapy to alleviate osteoarthritis.
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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.