ArticleCell proliferation2022
METTL3-m
Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 44 citations in OpenAlex.
- Mechanism study of METTL3 regulating Wnt/β-Catenin signalling in Pg.LPS-stimulated hSCAPs odontogenic differentiation.Molecular biology reports · 2026Article
- HDAC4 regulates hASC osteogenesis and bone regeneration by mediating SMAD4 via histone acetylation.Stem cell reports · 2026Article
- mMolecular medicine reports · 2026Review
- The YTHDC1-mInternational journal of oral science · 2026Article
- YTHDF3 Enhances Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in Osteoporosis by Promoting TBX19 Expression.Cell proliferation · 2026Article
- Engineered bone-targetingMaterials today. Bio · 2026Article
- Application Strategies of Bone Marrow Mesenchymal Stromal Cells in Bone-Related Diseases.Cell proliferation · 2026Review
- METTL3 inhibits LINC00312 to suppress osteoporosis progression in a YTHDF2‑dependent manner.International journal of molecular medicine · 2026Article
- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- Hypoxic BMSCs accelerate femur fracture healing via the METTL3/SLC2A3 m6A-glycolysis axis.Journal of translational medicine · 2025Article
- YTHDC1 Modulates the Osteogenic Capacity of hPDLSCs via Wnt/β-Catenin Signalling Pathway for the Treatment of Bone Defects in Osteoporosis Rats.Cell proliferation · 2025Article
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- METTL3-mediated m6A modification of circSTAT6 modulates miR-188-3p/Beclin1 axis to promote osteogenic differentiation of mesenchymal stem cells.Journal of orthopaedic surgery and research · 2025Article
- METTL3 regulated by histone lactylation promotes ossification of the ligamentum flavum by enhancing the m6A methylation of BMP2.Molecular medicine (Cambridge, Mass.) · 2025Article
- Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025Review
- Role of Wnt5a in modulation of osteoporotic adipose-derived stem cells and osteogenesis.Cell proliferation · 2025Article
- Epigenetic Mechanisms in Osteoporosis: Exploring the Power of mJournal of cellular and molecular medicine · 2025Review
- Unraveling the Role of N6-Methylation Modification: From Bone Biology to Osteoporosis.International journal of medical sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
objectivesBone marrow mesenchymal stem cells (BMSCs) hold a high osteogenic differentiation potential, but the mechanisms that control the osteogenic ability of BMSCs from osteoporosis (OP-BMSCs) need further research. The purpose of this experiment is to discuss the osteogenic effect of Mettl3 on OP-BMSCs and explore new therapeutic target that can enhance the bone formation ability of OP-BMSCs. MATERIALS AND
methodsThe bilateral ovariectomy (OVX) method was used to establish the SD rat OP model. Dot blots were used to reveal the different methylation levels of BMSCs and OP-BMSCs. Lentiviral-mediated overexpression of Mettl3 was applied in OP-BMSCs. QPCR and WB detected the molecular changes of osteogenic-related factors and Wnt signalling pathway in vitro experiment. The staining of calcium nodules and alkaline phosphatase detected the osteogenic ability of OP-BMSCs. Micro-CT and histological examination evaluated the osteogenesis of Mettl3 in OP rats in vivo.
resultsThe OP rat model was successfully established by OVX. Methylation levels and osteogenic potential of OP-BMSCs were decreased in OP-BMSCs. In vitro experiment, overexpression of Mettl3 could upregulate the osteogenic-related factors and activate the Wnt signalling pathway in OP-BMSCs. However, osteogenesis of OP-BMSCs was weakened by treatment with the canonical Wnt inhibitor Dickkopf-1. Micro-CT showed that the Mettl3(+) group had an increased amount of new bone formation at 8 weeks. Moreover, the results of histological staining were the same as the micro-CT results.
conclusionsTaken together, the methylation levels and osteogenic potential of OP-BMSCs were decreased in OP-BMSCs. In vitro and in vivo studies, overexpression of Mettl3 could partially rescue the decreased bone formation ability of OP-BMSCs by the canonical Wnt signalling pathway. Therefore, Mettl3 may be a key targeted gene for bone generation and therapy of bone defects in OP patients.
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.