Research shows oxygen levels influence retinal ganglion cell fate in optic nerve diseases, indicating potential for advanced models.
As the only output elements and projection neurons of the retina, the degeneration and death of retinal ganglion cells (RGCs) are key indicators of various optic nerve diseases affecting millions of people worldwide. During the embryonic development of the retina, oxygen (O₂) levels in the internal environment play a crucial role in the differentiation, migration, and maturation of RGCs. This article summarizes the impact of O₂ on RGC fate and its underlying mechanisms, based on the developmental temporal window of RGCs. It also compares the efficacy of commonly used animal models and human organoid models in simulating in vivo retinal development. Finally, the article emphasizes the importance of utilizing advanced techniques such as microfluidics and organoid chips in models to regulate O₂ levels more precisely. Additionally, combining traditional techniques like genetic perturbation and cell imaging with new technologies such as single-cell transcriptomics and CRISPR/Cas9 genome editing can enhance the depth of mechanism studies.
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Liu et al. (2025) studied this question.
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