ArticlePeerJ2023
CYP27A1 deficiency promoted osteoclast differentiation.
Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Mitochondria-related gene and protein changes in craniosynostosis: integrated transcriptomics and Fgfr2C361Y/+ cranial suture proteomics.Functional & integrative genomics · 2026Article
- Polygenic Prediction of Equestrian Sport Discipline Among Horses Bred for Jumping and Dressage.Animal genetics · 2026Article
- Myocyte-Specific Enhancer Factor 2A Potentiates Osteoclastic Differentiation in Osteoporosis by Inducing Endothelin Receptor Type A.Biochemical genetics · 2026Article
- Transcriptomics in the Study of Bone and Cartilage.Current osteoporosis reports · 2026Review
- Histological response of the periodontal tissue to mandibular incisor movement using clear aligners of varying thickness in a rabbit model.Korean journal of orthodontics · 2025Article
- NPC1L1 Drives Osteoporosis by Activating the C/EBPα/Cyp27a1/27-Hydroxycholesterol Axis: A Novel Therapeutic Target for Bone Loss.FASEB bioAdvances · 2025Article
- Multi-omics Analysis to Identify Key Immune Genes for Osteoporosis based on Machine Learning and Single-cell Analysis.Orthopaedic surgery · 2024Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The elevating osteoclast differentiation can lead to an imbalance in bone homeostasis, which was responsible for bone loss and bone diseases, such as osteoporosis. Multiple pathways and molecules have been involved in osteoclast formation, but the role of CYP27A1 in osteoclast differentiation has never been explored. Methods: CYP27A1 deficient mice were constructed using CRISPR-Cas9 system. Osteoclast differentiation was detected by TRAP staining. Differentially expressed genes (DEGs) were identified using RNA-seq analysis and were confirmed by qRT-PCR and Western blot. Results: The results showed that CYP27A1 knockout (KO) promoted osteoclast differentiation and bone loss. The transcriptomic analysis revealed that CYP27A1 KO led to differential expression of multiple genes, including ELANE, LY6C2, S100A9, GM20708, BGN, SPARC, and COL1A2, which were confirmed by qRT-PCR and Western blot. Enrichment analysis indicated that these differential genes were significantly associated with osteogenesis-related pathways, such as PPAR signaling, IL-17 signaling, and PI3K/AKT signaling, which were confirmed by qRT-PCR and Western blot. Conclusions: These results suggested that CYP27A1 was involved in osteoclast differentiation, providing a novel therapeutic target for osteoclast-related diseases.
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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.