Health Sciences Research and Teaching Center, Autonomous University of Sinaloa, Culiacan 80010, Sinaloa, Mexico.
Faculty of Dentistry, Autonomous University of Chihuahua, Chihuahua 31110, Chihuahua, Mexico.
Int J Mol Sci. 2023 Oct 16;24(20):15215. doi: 10.3390/ijms242015215.
The main complications causing practically 75% of all maternal deaths are severe bleeding, infections, and high blood pressure during pregnancy (preeclampsia (PE) and eclampsia). The usefulness of ncRNAs as clinical biomarkers has been explored in an extensive range of human diseases including pregnancy-related diseases such as PE. Immunological dysregulation show that the Th1/17:Th2/Treg ratio is "central and causal" to PE. However, there is evidence of the involvement of placenta-expressed miRNAs and lncRNAs in the immunological regulation of crucial processes of placenta development and function during pregnancy. Abnormal expression of these molecules is related to immune physiopathological processes that occur in PE. Therefore, this work aims to describe the importance of miRNAs and lncRNAs in immune dysregulation in PE. Interestingly, multiple ncRNAS are involved in the immune dysregulation of PE participating in type 1 immune response regulation, immune microenvironment regulation in placenta promoting inflammatory factors, trophoblast cell invasion in women with Early-Onset PE (EOPE), placental development, and angiogenesis, promotion of population of M1 and M2, proliferation, invasion, and migration of placental trophoblast cells, and promotion of invasion and autophagy through vias such as PI3K/AKT/mTOR, VEGF/VEGFR1, and TLR9/STAT3.
主要并发症导致实际上 75%的所有产妇死亡是严重出血、感染和高血压在怀孕期间（子痫前期（PE）和子痫）。ncRNAs 的有用性作为临床生物标志物已经在广泛的人类疾病包括妊娠相关疾病如 PE 进行了探索。免疫失调表明 Th1/17：Th2/Treg 比值是“中心和因果”对 PE。然而，有证据表明胎盘表达的 miRNAs 和 lncRNAs 参与了胎盘发育和功能的关键过程的免疫调节在怀孕期间。这些分子的异常表达与在 PE 中发生的免疫生理病理过程有关。因此，这项工作旨在描述 miRNA 和 lncRNAs 在 PE 免疫失调中的重要性。有趣的是，多个 ncRNAS 参与了 PE 的免疫失调参与 1 型免疫反应调节、胎盘促进炎症因子的免疫微环境调节、早发性子痫前期（EOPE）妇女的滋养细胞浸润、胎盘发育和血管生成、促进 M1 和 M2 细胞的增殖、滋养层细胞的侵袭和迁移，以及通过 PI3K/AKT/mTOR、VEGF/VEGFR1 和 TLR9/STAT3 等途径促进侵袭和自噬。
