Background

Neuroinflammation has been recognized as a key pathological event in acute glaucoma. Medical treatment of acute glaucoma has mainly focused on lowering intraocular pressure, yet the majority of patients still experience deterioration. Aberrant expression or activity of circular RNAs in the retina has been described in various ophthalmic diseases.

Objective

This study surveyed the mechanism of circRUFY1 in acute ocular hypertension (AOH)-induced retinal ganglion cell (RGC) injury.

Results

AOH rats expressed high circRUFY1 and CALM3, and low miR-196a-5p in the retina tissue. CircRUFY1 silencing in AOH-induced rats reduced the severity of retinal damage and RGC damage. CircRUFY1, as a ceRNA of miR-196a-5p, upregulated CALM3, and CALM3 overexpression could further activate the ERK pathway signaling in RGCs.

Conclusion

Silence of circRUFY1 protects RGCs from AOH injury mainly by inhibiting the ERK signaling pathway by regulating the miR-196a-5p/CALM3 axis. Overall, targeted intervention of circRUFY1 expression is a promising therapeutic strategy for treating RGC damage in acute glaucoma.

中文翻译：

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沉默circRUFY1通过miR-196a-5p/CALM3轴激活ERK通路保护急性高眼压时视网膜神经节细胞损伤

 背景

神经炎症已被认为是急性青光眼的关键病理事件。急性青光眼的治疗主要集中在降低眼压，但大多数患者的病情仍然恶化。视网膜中环状RNA的异常表达或活性已在多种眼科疾病中得到描述。

 客观的

本研究调查了 circRUFY1 在急性高眼压 (AOH) 诱导的视网膜神经节细胞 (RGC) 损伤中的机制。

 结果

AOH 大鼠视网膜组织中 circRUFY1 和 CALM3 表达高，miR-196a-5p 表达低。 AOH 诱导的大鼠中 CircRUFY1 沉默可减轻视网膜损伤和 RGC 损伤的严重程度。 CircRUFY1作为miR-196a-5p的ceRNA，上调CALM3，并且CALM3过表达可以进一步激活RGC中的ERK通路信号传导。

 结论

circRUFY1的沉默主要通过调节miR-196a-5p/CALM3轴来抑制ERK信号通路来保护RGC免受AOH损伤。总体而言，circRUFY1表达的靶向干预是治疗急性青光眼RGC损伤的一种有前景的治疗策略。