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JNK 抑制可改善视网膜色素变性小鼠模型中的 rod 光感受器变性。

Inhibition of JNK ameliorates rod photoreceptor degeneration in a mouse model of retinitis pigmentosa.

机构信息

Chinese Academy of Sciences Key Laboratory of Brain Connectome and Manipulation, Shenzhen Key Laboratory of Translational Research for Brain Diseases, Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.

Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen, China.

出版信息

FEBS Lett. 2024 Nov;598(21):2683-2701. doi: 10.1002/1873-3468.14978. Epub 2024 Jul 15.

Abstract

Retinitis pigmentosa (RP) is an inherited eye disease that causes progressive vision loss. Microglial activation and inflammation play essential roles in photoreceptor degeneration in RP, although the underlying mechanisms remain unclear. Here, we examined the progressive degeneration of photoreceptors in rd1 mice, a mouse model of RP. We investigated the molecular changes in various retinal cells in rd1 mice using single-cell RNA sequencing and found that potentiation of JNK signaling is associated with photoreceptor degeneration in RP. Moreover, inflammation-related molecules, which function downstream of JNK, are elevated in RP. Furthermore, inhibiting JNK alleviates microglial activation and rescues photoreceptor degeneration in rd1 mice. Thus, our findings suggest that targeting JNK is a promising approach for slowing RP progression.

摘要

色素性视网膜炎(RP)是一种遗传性眼病,可导致视力逐渐丧失。小胶质细胞激活和炎症在 RP 中的光感受器变性中起着重要作用,尽管其潜在机制尚不清楚。在这里,我们检查了 rd1 小鼠(一种 RP 小鼠模型)中光感受器的进行性变性。我们使用单细胞 RNA 测序研究了 rd1 小鼠各种视网膜细胞中的分子变化,发现 JNK 信号的增强与 RP 中的光感受器变性有关。此外,RP 中 JNK 下游的炎症相关分子升高。此外,抑制 JNK 可减轻 rd1 小鼠中的小胶质细胞激活并挽救光感受器变性。因此,我们的研究结果表明,靶向 JNK 可能是减缓 RP 进展的一种有前途的方法。

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