ArticleScientific reports2024
ALKBH5 regulates etoposide-induced cellular senescence and osteogenic differentiation in osteoporosis through mediating the m
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Milk-derived exosome-based strategy targeting ferroptosis-glycolysis network promotes bone regeneration in diabetic aging comorbidity.Journal of nanobiotechnology · 2026Article
- Epigenetic transcriptional regulation of skeletal aging: The emerging role of mJournal of orthopaedic translation · 2026Review
- Article
- Bone Marrow Mesenchymal Stem Cell Senescence in the Development of Osteoporosis: Mechanisms, Interventions, and Future Directions.Current molecular medicine · 2026Review
- ALKBH5/YTHDF2 Axis Regulates Osteogenic Differentiation Through Mediating the mInternational journal of endocrinology · 2026Article
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- FN9-10ELP, an ECM-Mimetic Fusion Protein, Protects Human Mesenchymal Stem Cells from Etoposide-Induced Senescence.International journal of molecular sciences · 2025Article
- The Senotherapeutic Effects of APPA (Apocynin [AP] and Paeonol [PA]) on Senescent Human Chondrocytes.Pharmaceuticals (Basel, Switzerland) · 2025Article
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- m6A: a novel strategy for osteoporosis treatment.Frontiers in cell and developmental biology · 2025Review
- Unraveling the Role of N6-Methylation Modification: From Bone Biology to Osteoporosis.International journal of medical sciences · 2025Review
- ALKBH5 in development: decoding the multifaceted roles of mFrontiers in molecular biosciences · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
Osteoporosis, a common bone disease in older individuals, involves the progression influenced by N6-methyladenosine (m6A) modification. This study aimed to elucidate the effects of VDAC3 m6A modification on human bone mesenchymal stromal cell (BMSC) senescence and osteogenic differentiation. BMSCs were treated with etoposide to induce senescence. Senescence was assessed by β-galactosidase staining and quantitative real-time PCR (qPCR), and osteogenic differentiation was evaluated using Western blot, alkaline phosphatase, and alizarin red S staining. VDAC3 and ALKBH5 expression were quantified by qPCR, and their interaction was assessed by RNA immunoprecipitation (RIP) and luciferase reporter assay. m6A methylation was analyzed using the Me-RIP assay. VDAC3 expression was significantly decreased in etoposide-treated BMSCs (1.00 ± 0.13 vs. 0.26 ± 0.06). VDAC3 overexpression reduced etoposide-induced senescence and promoted osteogenic differentiation. ALKBH5 overexpression inhibited VDAC3 m6A modification (1.00 ± 0.095 vs. 0.233 ± 0.177) and its stability. ALKBH5 knockdown decreased etoposide-induced senescence and promoted osteogenic differentiation, effects that were reversed by VDAC3 knockdown. YTHDF1 was identified as the m6A methylation reader, and its overexpression inhibited VDAC3 stability. We demonstrated that ALKBH5 inhibited osteogenic differentiation of etoposide-induced senescent cells through the inhibition of VDAC3 m6A modification, and YTHDF1 acted as the m6A methylation reader. These findings provide a novel theoretical basis for the treatment of osteoporosis.
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