ArticleCell death & disease2022
Downregulation of METTL14 improves postmenopausal osteoporosis via IGF2BP1 dependent posttranscriptional silencing of SMAD1.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 69 citations in OpenAlex.
- PDE4D Mediates the Cardiac Ischemia Reperfusion Injury and Is m6A Modified by METTL14.Korean circulation journal · 2026Article
- Epigenetic Regulation of Bone Homeostasis in Osteoporosis: Mechanisms, Evidence Gaps, and Translational Prospects.Cell biochemistry and function · 2026Review
- mMolecular medicine reports · 2026Review
- YTHDF3 Enhances Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in Osteoporosis by Promoting TBX19 Expression.Cell proliferation · 2026Article
- Expression Profile and Role of the IGF2BP1-3 Genes During Human in vitro Osteogenic Differentiation.Cell biochemistry and biophysics · 2026Article
- The FOXO3/ZC3H13/SLC3A2 cascade modulates the osteogenic differentiation and ferroptosis of BMSCs.Journal of bioenergetics and biomembranes · 2026Article
- Epigenetic transcriptional regulation of skeletal aging: The emerging role of mJournal of orthopaedic translation · 2026Review
- mInternational journal of molecular medicine · 2026Review
- Melatonin Counteracts Mechanical Unloading-Induced Bone Loss Through YTHDF3-Mediated mJournal of pineal research · 2026Article
- T-2 toxin induces degradation of chondrocytes extracellular matrix through the methyltransferase-like 3/m6A/Csf1 axis.Archives of toxicology · 2026Article
- METTL14/IGF2BP1 mInfection and immunity · 2026Article
- mStem cell research & therapy · 2026Article
- Integrative Proteogenomic Analysis Identifies Genetically Supported Plasma Proteins, Metabolites, and Pathways in Glaucoma.Investigative ophthalmology & visual science · 2026Article
- METTL14 Promotes the Osteogenic Differentiation of Human Bone Marrow Stromal Cells via m6A-Dependent Stabilization of USP7 mRNA.Biochemical genetics · 2026Article
- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- Alternating Current Stimulation Promotes Healing of Bone Fractures in Rabbits.Bioengineering (Basel, Switzerland) · 2025Article
- KIAA1429-mediated MCellular & molecular biology letters · 2025Article
- Methyltransferase-like 14 mediated FOXP1 m6A modification alleviates osteoporosis by regulating the Wnt/β-catenin pathway.Journal of molecular histology · 2025Article
- Accelerating Bone Healing With METTL3 Overexpressed Adipose-Derived Stem Cells in Osteoporotic Rats.Cell proliferation · 2025Article
- High-efficient discovering the potent anti-Notum agents from herbal medicines for combating glucocorticoid-induced osteoporosis.Acta pharmaceutica Sinica. B · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis (OP) tends to occur in postmenopausal women, making them prone to fractures. N6-methyladenosine (m6A) methylation plays a crucial role in OP. Herein, we aimed to explore the effects of METTL14 on osteogenesis and the underlying mechanism. Osteogenic differentiation was assessed through osteoblast markers expression, cell proliferation, ALP activity, and mineralization, which were detected by qRT-PCR, CCK-8, EdU assay, ALP staining assay, and ARS staining assay, respectively. Osteoporosis was evaluated in OVX mice using qRT-PCR, microcomputed tomography, and H&E staining assay. The levels of METTL14 and SMAD1 were measured using qRT-PCR and western blot, and their interaction was assessed using RIP and luciferase reporter assay. M6A methylation was analyzed using the Me-RIP assay. The results indicated that m6A, METTL14, and SMAD1 levels were downregulated in patients with OP and OVX mice, and upregulated in osteogenic BMSCs. Knockdown of METTL14 suppressed osteogenesis of BMSCs and reduced bone mass of OVX mice. Moreover, silencing of METTL14 positively related to SMAD1 and inhibited m6A modification of SMAD1 by suppressing its stability. IGF2BP1 was identified as the methylation reader, and which knockdown reversed the upregulation induced by SMAD1. Overexpression of SMAD1 reversed the suppression of osteogenic differentiation induced by METTL14 knockdown. In conclusion, interference with METTL14 inhibited osteogenic differentiation of BSMCs by m6A modification of SMAD1 in an IGFBP1 manner, suggesting that METTL14 might be a novel approach for improving osteoporosis.
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