ArticleNature communications2025
Piezo1-mediated mechanotransduction controls osteocyte maturation and dendrite development via a YAP-CCN-Src signaling axis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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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.
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Who cites it
22 citing papers in PubMed.
- Tibial bone compression promotes recovery after brain injury through osteocyte PIEZO1.Nature neuroscience · 2026Article
- Piezo1 in Peripheral and Central Sensitisation: Implications for Chronic Pain.Bioengineering (Basel, Switzerland) · 2026Review
- Piezo1-mediated Mechanotransduction in the musculoskeletal system: Signaling networks and therapeutic perspectives.Bone reports · 2026Review
- Mechanobiological feedback loops and quantitative decision thresholds in organ fibrosis: Translational principles for antifibrotic therapy.Journal of cell communication and signaling · 2026Review
- Decoding osteosarcoma mechanobiology: PIEZO channels in tumor progression, immune remodeling, and pain.Cancer metastasis reviews · 2026Review
- Matrix Competence Failure in Osteoporosis: Mechanosensing, Osteoimmune Crosstalk, and Fragility Beyond Bone Mineral Density.Current medical science · 2026Review
- Piezo1, Integrins, and YAP/TAZ in Osteoporotic Mechanotransduction: Key Pathways, Crosstalk, and Therapeutic Implications.Calcified tissue international · 2026Review
- Mechanobiology-Driven Metabolic Reprogramming: Integrative Roles of YAP/TAZ Signaling and Extracellular Matrix Dynamics.Cell biology international · 2026Review
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- BMAL1 Proteostasis, Circadian Dysfunction, and Ferroptotic Vulnerability in Osteoporosis: Current Evidence and Experimental Priorities.Calcified tissue international · 2026Review
- Recapitulating Endochondral Ossification for Bone Repair: From Development to Engineering Strategy.Advanced healthcare materials · 2026Review
- Coordinated Bone-Muscle Axis Association in South China Carp (Foods (Basel, Switzerland) · 2026Article
- Role of YAP/TAZ Mechanobiological Signaling in Osteoporosis and Osteoarthritis.Calcified tissue international · 2026Review
- Adjunct Tendon Vibration and Bone Outcomes in Older Adults with Osteoporosis: A 12-Month Prospective Cohort Study.Journal of clinical medicine · 2026Article
- CFTR mediates ClNature communications · 2026Article
- Osteocytes in the Metastatic Bone Niche: Mechanistic Pathways and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- New knock-in mouse linesJBMR plus · 2026Article
- Hydrostatic pressure promotes odontoblast differentiation via PIEZO1-dependent activation of RUNX2 and WNT16 in SHED.Scientific reports · 2026Article
- Bone matrix proteins: regulators of skeletal remodeling and repair.Journal of bone and mineral metabolism · 2026Review
- Black Phosphorus Nanomaterials and the Senescent Osteoimmune Microenvironment: Mechanisms, Opportunities, Challenges, and Future Outlook.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Mechanical force controls bone development and homeostasis, with mechanosensitive osteocytes playing a key role. Osteocytes form interconnected dendrites to respond to mechanical stimuli and regulate bone formation and resorption. However, the molecular mechanisms underlying osteocyte maturation and dendrite formation remain elusive. Here we show that Piezo1 loss in late osteoblasts and osteocytes reduces bone mass and disrupts osteocyte differentiation with reduced dendrite number, length and network formation. Decreased YAP activity and unexpected Wnt/β-catenin signaling activation cause these deficiencies, largely restored by intermittent YAP activation. We further identify YAP targets CCN1/2 as crucial secreted factors in the Piezo1-YAP mechanotransduction. CCN1/2 overexpression in the liver rescues dendritic and bone defects in the Piezo1 mutant mice by activating Src, promoting actin polymerization, and activating YAP in a positive feedforward loop. Our findings highlight the pivotal roles of Piezo1 and YAP-CCN1/2-Src signaling, offering potential therapeutic targets for improving osteocyte dendritic networks.
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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.