ArticleCell death discovery2024
METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- WTAP Transcriptional Suppression by KLF9 Drives Osteoclastogenesis via MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- mMolecular medicine reports · 2026Review
- Pancreatic β-cell aging in physiology and diabetes: emerging roles of m6A mRNA methylation.Journal of molecular endocrinology · 2026Review
- YTHDF3 Enhances Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in Osteoporosis by Promoting TBX19 Expression.Cell proliferation · 2026Article
- The Role of NMedComm · 2026Review
- 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
- m6A RNA modifications in neurosystem genes as early markers for osteoporosis with iron accumulation.Molecular biology reports · 2026Article
- E2F2 suppresses cell senescence and promotes odontogenic differentiation in dental pulp stem cells by stabilizing METTL3.Odontology · 2026Article
- mStem cell research & therapy · 2026Article
- Review
- YTHDF1 transcriptionally activated by TCF4 suppresses osteoblast ferroptosis in titanium nanoparticle-induced osteolysis by accelerating GPX4 and SLC7A11 translation.Journal of nanobiotechnology · 2025Article
- METTL3 safeguards cell identity and epigenome of human trophoblast stem cells.Nature communications · 2025Article
- Hypoxic BMSCs accelerate femur fracture healing via the METTL3/SLC2A3 m6A-glycolysis axis.Journal of translational medicine · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- FTO-mediated MMP1 m6A modification promotes osteogenic differentiation of bone marrow mesenchymal stem cells via the ERK pathway in congenital scoliosis.Scientific reports · 2025Article
- Cellular senescence and other age-related mechanisms in skeletal diseases.Bone research · 2025Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- mInternational journal of molecular sciences · 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
16 authors at 3 institutions in 1 country.
Funding
Abstract
Senile osteoporosis is mainly caused by osteoblasts attenuation, which results in reduced bone mass and disrupted bone remodeling. Numerous studies have focused on the regulatory role of m6A modification in osteoporosis; however, most of the studies have investigated the differentiation of bone marrow mesenchymal stem cells (BMSCs), while the direct regulatory mechanism of m6A on osteoblasts remains unknown. This study revealed that the progression of senile osteoporosis is closely related to the downregulation of m6A modification and methyltransferase-like 3 (METTL3). Overexpression of METTL3 inhibits osteoblast aging. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) revealed that METTL3 upregulates the stability of Hspa1a mRNA, thereby inhibiting osteoblast aging. Moreover, the results demonstrated that METTL3 enhances the stability of Hspa1a mRNA via m6A modification to regulate osteoblast aging. Notably, YTH N6-methyladenosine RNA binding protein 2 (YTHDF2) participates in stabilizing Hspa1a mRNA in the METTL3-mediated m6A modification process, rather than the well-known degradation function. Mechanistically, METTL3 increases the stability of Hspa1a mRNA in a YTHDF2-dependent manner to inhibit osteoblast aging. Our results confirmed the significant role of METTL3 in osteoblast aging and suggested that METTL3 could be a potential therapeutic target for senile osteoporosis.
Identifiers
What Socratic 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 Socratic graph.