ArticleProceedings of the National Academy of Sciences of the United States of America2025
Nat10-mediated N4-acetylcytidine modification enhances Nfatc1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Glycolysis in bone remodeling: from energy supply to signaling regulation.Molecular biology reports · 2026Review
- Article
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- The Role of NAT10-Mediated ac4C Modification in Osteoblast Function and Bone Formation: Insights from Integrative Bioinformatics and Experimental Validation.Physiological research · 2026Article
- Biomimetic hybrid nanocarriers hitchhike neutrophils for targeted ginsenoside Rc delivery to BMSCs: ameliorating postmenopausal osteoporosis via iron homeostasis regulation.Journal of nanobiotechnology · 2026Article
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- Nutritional Biomarkers, Bone Turnover, and Oxidative DNA Damage in Postmenopausal Women with Periodontitis: A Cross-Sectional Study.Nutrients · 2026Article
- NAT10 and ac4C modification in cancer immunity and metabolism: emerging mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- miR-326 promotes osteogenic differentiation of bone marrow mesenchymal stem cells by targeting NAT10.Journal of orthopaedic surgery and research · 2026Article
- Targeting NAT10 with Remodelin in cancer drug resistance: mechanisms, preclinical evidence, and combination strategies.Frontiers in pharmacology · 2026Review
- Research Hotspots and Emerging Trends in Osteoporosis Epigenetics.Genetics research · 2026Article
- Bone Marrow Immunometabolic Remodeling in Osteoporosis: From Systemic Risk Factors to Precision Intervention.International journal of general medicine · 2026Review
- Development and Validation of an UPLC-MS/MS Method for Remodelin Quantification in Mouse Plasma and Tissues: Application to Biodistribution and Ultrastructural Assessment.Journal of analytical methods in chemistry · 2026Article
- Nat10-mediated N4-acetylcytidine modification enhances Nfatc1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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18 authors.
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Abstract
Increased differentiation or activity of osteoclasts is the key pathogenic factor of postmenopausal osteoporosis (PMOP). N4-acetylcytidine (ac4C) modification, catalyzed by Nat10, is a novel posttranscriptional mRNA modification related to many diseases. However, its impact on regulating osteoclast activation in PMOP remains uncertain. Here, we initially observed that Nat10-mediated ac4C positively correlates with osteoclast differentiation of monocytes and low bone mass in PMOP. The specific knockout of Nat10 in monocytes and remodelin, a Nat10 inhibitor, alleviates ovariectomized (OVX)-induced bone loss by downregulating osteoclast differentiation. Mechanistically, epitranscriptomic analyses reveal that the nuclear factor of activated T cells cytoplasmic 1 (Nfatc1) is the key downstream target of ac4C modification during osteoclast differentiation. Subsequently, translatomic results demonstrate that Nat10-mediated ac4C enhances the translation efficiency (TE) of Nfatc1, thereby inducing Nfatc1 expression and consequent osteoclast maturation. Cumulatively, these findings reveal the promotive role of Nat10 in osteoclast differentiation and PMOP from a novel field of RNA modifications and suggest that Nat10 can be a target of epigenetic therapy for preventing bone loss in PMOP.
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