Abstract: Gestational diabetes mellitus (GDM), one of the most common complications during pregnancy, is associated with a high risk of short- and long-term adverse effects on the mother and offspring. Placenta-derived hormones and cytokines aggravate maternal insulin resistance (IR) during pregnancy, which in turn contribute to GDM. The hyperglycemia and IR in GDM result in aberrant placental structure and function adversely affecting fetal growth and well-being. Therefore, it is reasonable to assume that structural and functional alterations in the placenta contribute to the pathogenesis of GDM and GDM-related complications. Increasing evidence suggests that multiple non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs, and circular RNAs, are dysregulated in placentas of patients with GDM and linked to abnormal placental structure, metabolism, and function. Manipulation of ncRNA expression led to some key pathophysiological features of GDM, such as trophoblast dysfunction, changes in intracellular glucose metabolism, and inflammation. Moreover, placenta-specific ncRNAs may be potential diagnostic biomarkers and even therapeutic targets for GDM. This review summarizes data published on the involvement of aberrantly expressed placental ncRNAs in GDM and provides information on their role in the pathogenesis of GDM and GDM-associated complications.

Keywords: dysregulated ncRNA, pregnancy disorder, placental dysfunction, pregnancy-related complications, trophoblast dysfunction


中文翻译：

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胎盘中异常表达的非编码 RNA 及其在妊娠糖尿病病理生理学中的作用

摘要：妊娠期糖尿病 (GDM) 是妊娠期间最常见的并发症之一，与对母亲和后代产生短期和长期不良影响的高风险相关。胎盘衍生的激素和细胞因子会在怀孕期间加重母体胰岛素抵抗 (IR)，进而导致 GDM。GDM 中的高血糖和 IR 导致胎盘结构和功能异常，对胎儿的生长和健康产生不利影响。因此，假设胎盘的结构和功能改变有助于 GDM 和 GDM 相关并发症的发病机制是合理的。越来越多的证据表明，多种非编码 RNA (ncRNA)，包括 microRNA、长链非编码 RNA 和环状 RNA，在 GDM 患者的胎盘中失调，并与胎盘结构异常有关，新陈代谢, 功能. ncRNA 表达的操纵导致 GDM 的一些关键病理生理特征，例如滋养细胞功能障碍、细胞内葡萄糖代谢的变化和炎症。此外，胎盘特异性 ncRNA 可能是潜在的诊断生物标志物，甚至是 GDM 的治疗靶点。本综述总结了已发表的关于异常表达的胎盘 ncRNA 参与 GDM 的数据，并提供了有关它们在 GDM 发病机制和 GDM 相关并发症中的作用的信息。

关键词： ncRNA 失调，妊娠障碍，胎盘功能障碍，妊娠相关并发症，滋养细胞功能障碍