ArticleScientific reports2025
HIF-1α regulates the proliferation and differentiation of mouse cranial base sphenoid-occipital synchondrosis chondrocytes via PI3K/Akt signaling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The HIF-Mediated PI3K-AKT Signaling Pathway Is a Key Signaling Pathway Triggering Testicular Spermatogenic Disorders in Yaks with Cryptorchidism.Veterinary sciences · 2026Article
- Computational Mapping of Hedgehog Pathway Kinase Module Predicts Node-Specific Craniofacial Phenotypes.Genes · 2026Article
- Combination of hypoxia and hyperosmolarity reducesFrontiers in veterinary science · 2026Article
- The developing tendon and enthesis are hypoxic and rely on hypoxia-inducible factor 1a (bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
6 authors.
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Abstract
The cranial base synchondrosis (CBS) is a critical growth center in the craniofacial region, and its abnormal development can lead to various craniofacial deformities. In a hypoxic microenvironment, hypoxia-inducible factor-1α (HIF-1α) is a crucial regulatory factor for cellular adaptation to low oxygen conditions. However, the role of HIF-1α in the CBS and its mechanisms regulating the function of chondrocytes remain unclear. This study aims to investigate the expression characteristics of HIF-1α in the CBS and its potential mechanisms in regulating mouse spheno-occipital synchondrosis (SOS) chondrocytes (SOSCs). Histological and immunohistochemical staining were utilized to observe the growth pattern of the SOS and the expression characteristics of HIF-1α in the SOS of 1-8 week-old mice. Chemical hypoxia simulation and siRNA technology modulated HIF-1α expression, and potential signaling pathways were detected through transcriptome sequencing. Results indicate that HIF-1α is expressed in all layers of the mouse SOS and is closely associated with cell proliferation and differentiation. In vitro studies demonstrate that enhancing HIF-1α expression enhances cell proliferation and matrix synthesis capacity, improves cell apoptosis, and enhances the expression of chondrogenic markers SOX9 and Collagen II while diminishing osteogenic marker RUNX2 expression. We found that with the upregulation of HIF-1α expression, the PI3K/Akt signaling pathway is activated. In conclusion, our study revealed that HIF-1α regulates the proliferation and differentiation of SOSCs by activating the PI3K/Akt signaling pathway.
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