ArticleNature communications2016
EZH1 and EZH2 promote skeletal growth by repressing inhibitors of chondrocyte proliferation and hypertrophy.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- SkeletalVis: an exploration and meta-analysis data portal of cross-species skeletal transcriptomics data.Bioinformatics (Oxford, England) · 2019Pooled it
- Aggrecan deficiency does not increase susceptibility to estrogen-induced growth plate senescence.Journal of the Endocrine Society · 2026Article
- The Trajectory of Epigenetic Chromatin Remodeling in Cardiometabolic Disease and its Therapeutic Implications.Journal of cardiovascular translational research · 2026Review
- Enhancer of zeste homolog 2 (Ezh2) is required in mouse Isl1-expressing progenitors for proper development of cardiac and skeletal hindlimb structures.Biology open · 2026Article
- Molecular and Chromatin Accessibility Programs Underlying Epithelial Injury and Impaired Regeneration in Neonatal Necrotizing Enterocolitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- A Functional Shift of IGFBP3 in Osteoarthritis: From Cartilage Protection to Disease Promotion.Journal of inflammation research · 2026Review
- The genetic basis of human height.Nature reviews. Genetics · 2025Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Repair mechanisms of bone system tissues based on comprehensive perspective of multi-omics.Cell biology and toxicology · 2025Review
- Matrix stiffness aggravates osteoarthritis progression through H3K27me3 demethylation induced by mitochondrial damage.iScience · 2024Article
- Epigenetic Priming Enhances Chondrogenic Potential of Expanded Chondrocytes.Tissue engineering. Part A · 2024Article
- Growth disorders caused by variants in epigenetic regulators: progress and prospects.Frontiers in endocrinology · 2024Review
- Prenatal and Neonatal Bone Health: Updated Review on Early Identification of Newborns at High Risk for Osteopenia.Nutrients · 2023Review
- Genome-wide CRISPR screening of chondrocyte maturation newly implicates genes in skeletal growth and height-associated GWAS loci.Cell genomics · 2023Article
- Article
- Mechanical memory stored through epigenetic remodeling reduces cell therapeutic potential.Biophysical journal · 2023Article
- Rare diseases of epigenetic origin: Challenges and opportunities.Frontiers in genetics · 2023Review
- A critical bioenergetic switch is regulated by IGF2 during murine cartilage development.Communications biology · 2022Article
- Growing Pains: The Need for Engineered Platforms to Study Growth Plate Biology.Advanced healthcare materials · 2022Review
- MicroRNA-101a enhances trabecular bone accrual in male mice.Scientific reports · 2022Article
6 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
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Histone methyltransferases EZH1 and EZH2 catalyse the trimethylation of histone H3 at lysine 27 (H3K27), which serves as an epigenetic signal for chromatin condensation and transcriptional repression. Genome-wide associated studies have implicated EZH2 in the control of height and mutations in EZH2 cause Weaver syndrome, which includes skeletal overgrowth. Here we show that the combined loss of Ezh1 and Ezh2 in chondrocytes severely impairs skeletal growth in mice. Both of the principal processes underlying growth plate chondrogenesis, chondrocyte proliferation and hypertrophy, are compromised. The decrease in chondrocyte proliferation is due in part to derepression of cyclin-dependent kinase inhibitors Ink4a/b, while ineffective chondrocyte hypertrophy is due to the suppression of IGF signalling by the increased expression of IGF-binding proteins. Collectively, our findings reveal a critical role for H3K27 methylation in the regulation of chondrocyte proliferation and hypertrophy in the growth plate, which are the central determinants of skeletal growth.
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.