ArticleNature communications2020
A FAK/HDAC5 signaling axis controls osteocyte mechanotransduction.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 85 citations in OpenAlex.
- N-Terminal Basic Helix and S120 Phosphorylation Cooperatively Regulate Nuclear Localization of UBE2A/B in Mechanotransduction.Biology · 2026Article
- Three-dimensional niche-like porous structure locoregionally regulating macrophage immunosenescence rejuvenates aged bone repair.Bioactive materials · 2026Article
- Regulation of cAMP levels in osteocytes by mechano-sensitive focal adhesion kinase and phosphodiesterase 8A.iScience · 2026Article
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- ECM-Stiffness Mediated Persistent Fibroblast Activation Requires Integrin and Formin Dependent Chromatin Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- Focal Adhesion Kinase Promotes Calcification of Vascular Smooth Muscle Cells via Regulation of Histone Deacetylase 4 and 5.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Piezoelectric Biomaterials for Bone Regeneration: Roadmap from Dipole to Osteogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- UTX Responds to Nanotopography to Suppress Macrophage Inflammatory Response by Remodeling H3K27me3 Modification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Differential gene expression in trabecular bone osteocytes is related to the local strain and strain gradient.Scientific reports · 2025Article
- Modulation of Gene Expression by Substrate Stiffness via Ubiquitination of Histone H2B by Ubiquitin-Conjugating Enzyme E2A/B.ACS omega · 2025Article
- Optogenetic activation of mechanical nociceptions to enhance implant osseointegration.Nature communications · 2025Article
- Mechanical Loading Induces NRF2 Nuclear Translocation to Epigenetically Remodel Oxidative Stress Defense in Osteocytes.Antioxidants (Basel, Switzerland) · 2025Article
- Unlocking the Epigenetic Symphony: Histone Acetylation Orchestration in Bone Remodeling and Diseases.Stem cell reviews and reports · 2025Review
- FAK inhibition disrupts tumor growth, apoptosis, and transcriptional regulation in GI-NETs.Endocrine oncology (Bristol, England) · 2025Article
- Non-coding RNAs mediate mechanical load-regulating bone metabolic homeostasis.Frontiers in cell and developmental biology · 2025Review
- Osteocytes function as biomechanical signaling hubs bridging mechanical stress sensing and systemic adaptation.Frontiers in physiology · 2025Review
- Systems-level reconstruction of kinase phosphosignaling networks regulating endothelial barrier integrity using temporal data.NPJ systems biology and applications · 2024Article
- PTH receptor signalling, osteocytes and bone disease induced by diabetes mellitus.Nature reviews. Endocrinology · 2024Review
- A biodegradable magnesium phosphate cement incorporating chitosan and rhBMP-2 designed for bone defect repair.Journal of orthopaedic translation · 2024Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
Osteocytes, cells ensconced within mineralized bone matrix, are the primary skeletal mechanosensors. Osteocytes sense mechanical cues by changes in fluid flow shear stress (FFSS) across their dendritic projections. Loading-induced reductions of osteocytic Sclerostin (encoded by Sost) expression stimulates new bone formation. However, the molecular steps linking mechanotransduction and Sost suppression remain unknown. Here, we report that class IIa histone deacetylases (HDAC4 and HDAC5) are required for loading-induced Sost suppression and bone formation. FFSS signaling drives class IIa HDAC nuclear translocation through a signaling pathway involving direct HDAC5 tyrosine 642 phosphorylation by focal adhesion kinase (FAK), a HDAC5 post-translational modification that controls its subcellular localization. Osteocyte cell adhesion supports FAK tyrosine phosphorylation, and FFSS triggers FAK dephosphorylation. Pharmacologic FAK catalytic inhibition reduces Sost mRNA expression in vitro and in vivo. These studies demonstrate a role for HDAC5 as a transducer of matrix-derived cues to regulate cell type-specific gene expression.
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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 Socratic graph.