Beijing Municipal Key Laboratory of Child Development and Nutriomics, Translational Medicine Laboratory, Capital Institute of Pediatrics, Beijing 100020, China.
Int J Mol Sci. 2023 Jan 22;24(3):2220. doi: 10.3390/ijms24032220.
Neural tube defects (NTDs) are complex congenital malformations resulting from failure of neural tube closure during embryogenesis, which is affected by the interaction of genetic and environmental factors. It is well known that folate deficiency increases the incidence of NTDs; however, the underlying mechanism remains unclear. Folate deficiency not only causes DNA hypomethylation, but also blocks the synthesis of 2'-deoxythymidine-5'-monophosphate (dTMP) and increases uracil misincorporation, resulting in genomic instabilities such as base mismatch, DNA breakage, and even chromosome aberration. DNA repair pathways are essential for ensuring normal DNA synthesis, genomic stability and integrity during embryonic neural development. Genomic instability or lack of DNA repair has been implicated in risk of development of NTDs. Here, we reviewed the relationship between folate deficiency, DNA repair pathways and NTDs so as to reveal the role and significance of DNA repair system in the pathogenesis of NTDs and better understand the pathogenesis of NTDs.
神经管缺陷(NTDs)是一种复杂的先天性畸形,是由于胚胎发生过程中神经管闭合失败所致,受遗传和环境因素相互作用的影响。众所周知,叶酸缺乏会增加 NTDs 的发病率;然而,其潜在的机制尚不清楚。叶酸缺乏不仅导致 DNA 低甲基化,还会阻断 2'-脱氧胸苷-5'-单磷酸(dTMP)的合成,并增加尿嘧啶错误掺入,导致碱基错配、DNA 断裂甚至染色体畸变等基因组不稳定性。DNA 修复途径对于在胚胎神经发育过程中确保正常的 DNA 合成、基因组稳定性和完整性至关重要。基因组不稳定性或缺乏 DNA 修复与 NTDs 的发病风险有关。在这里,我们综述了叶酸缺乏、DNA 修复途径与 NTDs 之间的关系,以揭示 DNA 修复系统在 NTDs 发病机制中的作用和意义,并更好地理解 NTDs 的发病机制。