BACKGROUND A study has shown that miR-423-5p is highly expressed in proliferative diabetic retinopathy. However, the exact biological functions and mechanisms of miR-423-5p in diabetic retinopathy (DR) progression are currently unclear. This study aimed to investigate the role of miR-423-5p in DR and the underlying mechanism. RESULTS Our data demonstrate that the expression of miR-423-5p is significantly increased in HG-induced RPE cells and DR patient plasma. Moreover, the overexpression of miR-423-5p exacerbates HG-induced apoptosis. Mechanistically, our results provide evidence that miR-423-5p directly targets TFF1. MiR-423-5p exerts its effect on HG-induced apoptosis in RPE cells through TFF1, and the NF-κB pathway is involved in the regulatory mechanism. Further analysis revealed that the transcription factor NFE2 regulates miR-423-5p promoter activity. In addition, NFE2 regulates the levels of TFF1 and NF-κB pathway-associated proteins by regulating the expression of miR-423-5p. CONCLUSION The NFE2-miR-423-5p-TFF1 axis is a novel molecular mechanism and provides a new direction for the study and treatment of DR.

中文翻译：

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NFE2 / miR-423-5p / TFF1轴调节视网膜色素上皮细胞中高葡萄糖诱导的凋亡。

背景研究表明，miR-423-5p在增生性糖尿病性视网膜病中高表达。但是，目前尚不清楚miR-423-5p在糖尿病性视网膜病变（DR）进展中的确切生物学功能和机制。这项研究旨在调查miR-423-5p在DR中的作用及其潜在机制。结果我们的数据表明，miR-423-5p的表达在HG诱导的RPE细胞和DR患者血浆中显着增加。此外，miR-423-5p的过表达加剧了HG诱导的细胞凋亡。从机理上讲，我们的结果提供了miR-423-5p直接靶向TFF1的证据。MiR-423-5p通过TFF1对RPE细胞中HG诱导的细胞凋亡发挥作用，而NF-κB通路参与调节机制。进一步的分析表明，转录因子NFE2调节miR-423-5p启动子活性。此外，NFE2通过调节miR-423-5p的表达来调节TFF1和NF-κB通路相关蛋白的水平。结论NFE2-miR-423-5p-TFF1轴是一种新型的分子机制，为DR的研究和治疗提供了新的方向。