ArticleScientific reports2023
Essentiality of Nfatc1 short isoform in osteoclast differentiation and its self-regulation.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
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- Dusp1 in osteolytic diseases-mechanisms and therapeutic potential.Scientific reports · 2025Article
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- Induction of HMOX1 by mesenchymal stem cell cytotherapy inhibits osteoclastogenesis and myeloma-induced bone disease.Clinical and translational medicine · 2025Article
- Neoandrographolide inhibits mature osteoclast differentiation to alleviate bone loss and treat osteoporosis.Frontiers in pharmacology · 2025Article
- DLK1 regulates periodontal inflammation by inhibiting NF-κB p65 and JNK signaling pathways.Odontology · 2025Article
- Bone-Targeted Fluoropeptide Nanoparticle Inhibits NF-κB Signaling to Treat Osteosarcoma and Tumor-Induced Bone Destruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exploring capsaicin as a multi-target agent for osteoporosis through computational insights.In silico pharmacology · 2025Article
- The Role of Rosavin in the Pathophysiology of Bone Metabolism.International journal of molecular sciences · 2024Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During osteoclast differentiation, the expression of the transcription factor nuclear factor of activated T cell 1 (Nfatc1) increases in an autoproliferative manner. Nfatc1 isoforms are of three sizes, and only the short isoform increases during osteoclast differentiation. Genetic ablation of the whole Nfatc1 gene demonstrated that it is essential for osteoclastogenesis; however, the specific role of the Nfatc1 short form (Nfatc1/αA) remains unknown. In this study, we engineered Nfatc1 short form-specific knockout mice and found that these mice died in utero by day 13.5. We developed a novel osteoclast culture system in which hematopoietic stem cells were cultured, proliferated, and then differentiated into osteoclasts in vitro. Using this system, we show that the Nfatc1/αA isoform is essential for osteoclastogenesis and is responsible for the expression of various osteoclast markers, the Nfatc1 short form itself, and Nfatc1 regulators.
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