| Autor: |
Li, Chang-Ping, Wu, Shen, Sun, Yong-Quan, Peng, Xue-Qi, Gong, Maolei, Du, Hong-Zhen, Zhang, Jingxue, Teng, Zhao-Qian, Wang, Ningli, Liu, Chang-Mei |
| Zdroj: |
Cell Reports Medicine; May 2024, Vol. 5 Issue: 5 |
| Abstrakt: |
The axons of retinal ganglion cells (RGCs) form the optic nerve, transmitting visual information from the eye to the brain. Damage or loss of RGCs and their axons is the leading cause of visual functional defects in traumatic injury and degenerative diseases such as glaucoma. However, there are no effective clinical treatments for nerve damage in these neurodegenerative diseases. Here, we report that LIM homeodomain transcription factor Lhx2promotes RGC survival and axon regeneration in multiple animal models mimicking glaucoma disease. Furthermore, following N-methyl-D-aspartate (NMDA)-induced excitotoxicity damage of RGCs, Lhx2mitigates the loss of visual signal transduction. Mechanistic analysis revealed that overexpression of Lhx2supports axon regeneration by systematically regulating the transcription of regeneration-related genes and inhibiting transcription of Semaphorin 3C (Sema3C). Collectively, our studies identify a critical role of Lhx2in promoting RGC survival and axon regeneration, providing a promising neural repair strategy for glaucomatous neurodegeneration. |
| Databáze: |
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