ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018
Skeletal cell YAP and TAZ combinatorially promote bone development.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07759466 (Hippo Signaling Pathway Proteins and Their Correlation With Markers of Apoptosis and Bone Metabolism in the Gingival Crevicular Fluid of Individuals With Periodontal Disease), which is not on this map. Cited by 108 papers.
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.
Hippo Signaling Pathway Proteins and Their Correlation With Markers of Apoptosis and Bone Metabolism in the Gingival Crevicular Fluid of Individuals With Periodontal Disease
Who cites it
108 citing papers in PubMed, 178 citations in OpenAlex.
- Mechanical control in dental and jaw morphogenesis and remodeling.International journal of oral science · 2026Review
- Yap1 regulates motility and vertebral development and prevents kyphoscoliosis in zebrafish.PLoS genetics · 2026Article
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- LATS1/2 Inhibitor Attenuates Osteoclast Differentiation via Hippo-YAP/TAZ Signaling Pathway and Alleviates Osteoporosis in Ovariectomized Rats.Current medical science · 2026Article
- Application of Intracellular Vesicles Surpass Extracellular Vesicles in Regenerative Repair of Inflammatory Bone Defects via the LAMA4-Mediated YAP/TAZ Signalling.Journal of extracellular vesicles · 2026Article
- Bone and muscle crosstalk in steroid-induced osteonecrosis of the femoral head: a four-axis pathophysiological framework.Frontiers in immunology · 2026Review
- Crosstalk between YAP/TAZ and ERα in mechanical and hormonal signaling in the skeletal system.Acta biochimica et biophysica Sinica · 2025Review
- Oxidative stress activates YAP/TEAD1/NCOA4 axis to promote ferroptosis of endplate chondrocytes and aggravate intervertebral disc degeneration.Journal of orthopaedic translation · 2025Article
- M2c Macrophages Mediate YAP1 to Promote Vascularized Bone Regeneration in Distraction Osteogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- YAP regulates transcriptional programs for layer-specific periosteal expansion during fracture repair.Science advances · 2025Article
- CYR61 delivery promotes angiogenesis during bone fracture repair.NPJ Regenerative medicine · 2025Article
- Metformin ameliorates osteoporosis by enhancing bone angiogenesis via the YAP1/TAZ-HIF1α axis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Extracellular matrix: Dystroglycan interactions-Roles for the dystrophin-associated glycoprotein complex in skeletal tissue dynamics.International journal of experimental pathology · 2025Review
- Role of YAP/TAZ in bone diseases: A transductor from mechanics to biology.Journal of orthopaedic translation · 2025Review
- FAK mediates mechanical signaling to maintain epithelial homeostasis through YAP/TAZ-TEADs.Histochemistry and cell biology · 2025Article
- Biophysical stimuli for promoting bone repair and regeneration.Medical review (2021) · 2025Review
- Spatial transcriptomics in bone mechanomics: Exploring the mechanoregulation of fracture healing in the era of spatial omics.Science advances · 2025Article
- Inhibition of Mitochondrial Fission Reverses Simulated Microgravity-Induced Osteoblast Dysfunction by Enhancing Mechanotransduction and Epigenetic Modification.Research (Washington, D.C.) · 2025Article
- Review
- Inflammation and mechanical force-induced bone remodeling.Periodontology 2000 · 2024Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The functions of the paralogous transcriptional coactivators Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) in bone are controversial. Each has been observed to promote or inhibit osteogenesis in vitro, with reports of both equivalent and divergent functions. Their combinatorial roles in bone physiology are unknown. We report that combinatorial YAP/TAZ deletion from skeletal lineage cells, using Osterix-Cre, caused an osteogenesis imperfecta-like phenotype with severity dependent on allele dose and greater phenotypic expressivity with homozygous TAZ vs. YAP ablation. YAP/TAZ deletion decreased bone accrual and reduced intrinsic bone material properties through impaired collagen content and organization. These structural and material defects produced spontaneous fractures, particularly in mice with homozygous TAZ deletion and caused neonatal lethality in dual homozygous knockouts. At the cellular level in vivo, YAP/TAZ ablation reduced osteoblast activity and increased osteoclast activity, in an allele dose-dependent manner, impairing bone accrual and remodeling. Transcriptionally, YAP/TAZ deletion and small-molecule inhibition of YAP/TAZ interaction with the transcriptional coeffector TEAD reduced osteogenic and collagen-related gene expression, both in vivo and in vitro. These data demonstrate that YAP and TAZ combinatorially promote bone development through regulation of osteoblast activity, matrix quality, and osteoclastic remodeling.-Kegelman, C. D., Mason, D. E., Dawahare, J. H., Horan, D. J., Vigil, G. D., Howard, S. S., Robling, A. G., Bellido, T. M., Boerckel, J. D. Skeletal cell YAP and TAZ combinatorially promote bone development.
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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.