ArticleMolecular endocrinology (Baltimore, Md.)2013
HDAC7 inhibits osteoclastogenesis by reversing RANKL-triggered β-catenin switch.
Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
29 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Differential Gene Expression Involved in Bone Turnover of Mice Expressing Constitutively Active TGFβ Receptor Type I.International journal of molecular sciences · 2024Article
- HDAC7: a promising target in cancer.Frontiers in oncology · 2024Review
- MiRNAs regulate cell communication in osteogenesis-angiogenesis coupling during bone regeneration.Molecular biology reports · 2023Review
- Histone deacetylase 7: a signalling hub controlling development, inflammation, metabolism and disease.The FEBS journal · 2023Review
- Comprehensive analysis of epigenetics mechanisms in osteoporosis.Frontiers in genetics · 2023Review
- FTY720 Attenuates LPS-Induced Inflammatory Bone Loss by Inhibiting Osteoclastogenesis via the NF-Journal of immunology research · 2023Article
- Article
- Knockdown of HDAC9 Inhibits Osteogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells Partially by Suppressing the MAPK Signaling Pathway.Clinical interventions in aging · 2022Article
- Article
- Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.International journal of molecular sciences · 2021Review
- Article
- Expression of histone deacetylase (HDAC) family members in bortezomib-refractory multiple myeloma and modulation by panobinostat.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- The Role of Epigenomics in Osteoporosis and Osteoporotic Vertebral Fracture.International journal of molecular sciences · 2020Review
- Epigenetic Regulators Involved in Osteoclast Differentiation.International journal of molecular sciences · 2020Review
- Loss of myocyte enhancer factor 2 expression in osteoclasts leads to opposing skeletal phenotypes.Bone · 2020Article
- Impaired autophagy triggered by HDAC9 in mesenchymal stem cells accelerates bone mass loss.Stem cell research & therapy · 2020Article
- Hepatic Osteodystrophy-Molecular Mechanisms Proposed to Favor Its Development.International journal of molecular sciences · 2019Review
- Regulation of Osteoclast Differentiation and Skeletal Maintenance by Histone Deacetylases.Molecules (Basel, Switzerland) · 2019Review
- HDAC6 regulates dental mesenchymal stem cells and osteoclast differentiation.BMC oral health · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The bone-resorbing osteoclast is essential for skeletal remodeling, yet its deregulation contributes to diseases such as osteoporosis and cancer bone metastasis. Here we identify histone deacetylase 7 (HDAC7) as a key negative regulator of osteoclastogenesis and bone resorption using both in vitro cellular and molecular analyses and in vivo characterization of conditional HDAC7-knockout mice. Bone marrow osteoclast differentiation assays reveal that HDAC7 overexpression suppresses, whereas HDAC7 deletion enhances, osteoclastogenesis. Mechanistically, in the absence of receptor activator of nuclear factor κ-B ligand (RANKL), HDAC7 attenuates β-catenin function and cyclin D1 expression, thereby reducing precursor proliferation; upon RANKL activation, HDAC7 suppresses NFATc1 and prevents β-catenin down-regulation, thereby blocking osteoclast differentiation. Consequently, HDAC7 deletion in the osteoclast lineage results in a 26% reduction in bone mass (P = 0.003) owing to 102% elevated bone resorption (P = 0.01). These findings are clinically significant in light of the remarkable therapeutic potentials of HDAC inhibitors for several diseases such as cancer, diabetes, and neurodegeneration.
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.