ArticleCell proliferation2022
Alkbh1-mediated DNA N6-methyladenine modification regulates bone marrow mesenchymal stem cell fate during skeletal aging.
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, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- mMolecular medicine reports · 2026Review
- Exosome-derived LncRNAs in bone remodeling: recent advances and future directions for bone disease therapy.Stem cell research & therapy · 2026Review
- Identification and Characterization of sQTLs and eQTLs Associated with Growth Traits in Yellow-Feathered Broilers.Poultry science · 2026Article
- The methyltransferase N6amt1 regulates hippocampal neurogenesis through 6 mA modification of Txnrd3 DNA.Cellular and molecular life sciences : CMLS · 2025Article
- Bidirectional regulation factor of bone marrow mesenchymal stromal cells differentiation: a focus on bone-fat balance in osteoporosis.Stem cell research & therapy · 2025Review
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- Biological interpretation of DNA/RNA modification by ALKBH proteins and their role in human cancer.European journal of medical research · 2025Review
- LncRNA NEAT1-206 regulates autophagy of human umbilical cord mesenchymal stem cells through the WNT5A/CaNon-coding RNA research · 2025Article
- Accumulation of advanced oxidation protein products aggravates bone-fat imbalance during skeletal aging.Journal of orthopaedic translation · 2025Article
- m6A: a novel strategy for osteoporosis treatment.Frontiers in cell and developmental biology · 2025Review
- ALKBH1: emerging biomarker and therapeutic target for cancer treatment.Discover oncology · 2024Review
- LEP O-GlcNAcylation inactivates NF-κB pathway by suppressing LEP protein level and thus mediates cellular senescence and osteogenic differentiation in mouse mesenchymal stem cells.BMC molecular and cell biology · 2024Article
- Syringin protects high glucose-induced BMSC injury, cell senescence, and osteoporosis by inhibiting JAK2/STAT3 signaling.Journal of applied biomedicine · 2024Article
- The Role of Mitochondrial Homeostasis in Mesenchymal Stem Cell Therapy-Potential Implications in the Treatment of Osteogenesis Imperfecta.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Rejuvenation of BMSCs senescence by pharmacological enhancement of TFEB-mediated autophagy alleviates aged-related bone loss and extends lifespan in middle aged mice.Bone research · 2024Article
- The role of m6A in angiogenesis and vascular diseases.iScience · 2024Review
- Optimization strategies for mesenchymal stem cell-based analgesia therapy: a promising therapy for pain management.Stem cell research & therapy · 2024Review
- Unraveling Key mOrthopaedic surgery · 2024Article
- METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.Cell death discovery · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
objectivesDNA N6-methyladenine (N6-mA) demethylase Alkbh1 participates in regulating osteogenic differentiation of mesenchymal stem cell (MSCs) and vascular calcification. However, the role of Alkbh1 in bone metabolism remains unclear. MATERIALS AND
methodsBone marrow mesenchymal stem cells (BMSCs)-specific Alkbh1 knockout mice were used to investigate the role of Alkbh1 in bone metabolism. Western blot, qRT-PCR, and immunofluorescent staining were used to evaluate the expression of Alkbh1 or optineurin (optn). Micro-CT, histomorphometric analysis, and calcein double-labeling assay were used to evaluate bone phenotypes. Cell staining and qRT-PCR were used to evaluate the osteogenic or adipogenic differentiation of BMSCs. Dot blotting was used to detect the level of N6-mA in genomic DNA. Chromatin immunoprecipitation (Chip) assays were used to identify critical targets of Alkbh1. Alkbh1 adeno-associated virus was used to overexpress Alkbh1 in aged mice.
resultsAlkbh1 expression in BMSCs declined during aging. Knockout of Alkbh1 promoted adipogenic differentiation of BMSCs while inhibited osteogenic differentiation. BMSC-specific Alkbh1 knockout mice exhibited reduced bone mass and increased marrow adiposity. Mechanistically, we identified optn as the downstream target through which Alkbh1-mediated DNA m6A modification regulated BMSCs fate. Overexpression of Alkbh1 attenuated bone loss and marrow fat accumulation in aged mice.
conclusionsOur findings demonstrated that Alkbh1 regulated BMSCs fate and bone-fat balance during skeletal aging and provided a potential target for the treatment of osteoporosis.
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.