ArticleCell proliferation2025
Accelerating Bone Healing With METTL3 Overexpressed Adipose-Derived Stem Cells in Osteoporotic Rats.
Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Effects of the Total Flavonoids fromCurrent molecular medicine · 2026Article
- Accelerating Bone Healing With METTL3 Overexpressed Adipose-Derived Stem Cells in Osteoporotic Rats.Cell proliferation · 2025Article
- METTL3-Mediated m6A Modification Enhances the Function of Adipose-Derived Stem Cells Under Hypoxic Conditions Thereby Improving Fat Graft Retention.Stem cells international · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
The treatment of postmenopausal osteoporosis (OP) presents a multifaceted challenge. Nonetheless, emerging research indicates a significant association between the N6-methyladenosine (m6A) methylase METTL3 and osteogenesis in OP. To investigate Mettl3's impact on osteogenic potential and the underlying molecular mechanisms, an OP rat model was established via ovariectomy (OVX). Osteoporotic adipose-derived stem cells (OP-ASCs) were then isolated. Results indicated a significant downregulation of Mettl3 expression in OP-ASCs. Subsequently, OP-ASCs were transfected with overexpressed Mettl3 lentivirus and treated for Dickkopf-related protein-1 (DKK1). Overexpression of the Mettl3 gene led to increased levels of osteogenic factors. DKK1 attenuated osteoblastic differentiation capacity in the Mettl3 overexpression group by inhibiting the Wnt signalling pathway. Consistent results were observed in vivo experiments. In conclusion, overexpression of Mettl3 promotes osteogenesis in OP-ASCs by activating the Wnt/β-catenin pathway.
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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.