Failure of neural tube closure resulting from excessive apoptosis leads to neural tube defects (NTDs). NADPH oxidase 4 (NOX4) is a critical mediator of cell growth and death, yet its role in NTDs has never been characterized. NOX4 is a potential target of miR‐322, and we have previously demonstrated that miR‐322 was involved in high glucose‐induced NTDs. In this study, we investigated the effect of NOX4 on the embryonic neuroepithelium in NTDs and reveal a new regulatory mechanism for miR‐322 that disrupts neurulation by ameliorating cell apoptosis.

中文翻译：

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miR-322 治疗通过沉默 NADPH 氧化酶 4 来挽救细胞凋亡和神经管缺陷形成。


过度细胞凋亡导致神经管闭合失败，导致神经管缺陷（NTD）。 NADPH 氧化酶 4 (NOX4) 是细胞生长和死亡的关键介质，但其在 NTD 中的作用从未被表征。 NOX4 是 miR-322 的潜在靶标，我们之前已经证明 miR-322 参与高糖诱导的 NTD。在这项研究中，我们研究了 NOX4 对 NTD 胚胎神经上皮的影响，并揭示了 miR-322 的一种新调节机制，该机制通过改善细胞凋亡来破坏神经形成。