Meng Yizi, Meng Yimei, Li Linli, Li Yuan, He Jin, Shan Yanhong
Department of Obstetrics, Obstetrics and Gynecology Center, The First Hospital of Jilin University, Changchun, China.
Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Front Cell Dev Biol. 2024 Dec 3;12:1494072. doi: 10.3389/fcell.2024.1494072. eCollection 2024.
Preeclampsia (PE) is a prevalent and multifaceted pregnancy disorder, characterized by high blood pressure, edema, proteinuria, and systemic organ dysfunction. It remains one of the leading causes of pregnancy complications, yet its exact origins and pathophysiological mechanisms are not fully understood. Currently, the only definitive treatment is delivery, often requiring preterm termination of pregnancy, which increases neonatal and maternal morbidity and mortality rates, particularly in severe cases. This highlights the urgent need for further research to elucidate its underlying mechanisms and develop targeted interventions. PE is thought to result from a combination of factors, including inflammatory cytokines, trophoblast dysfunction, and environmental influences, which may trigger epigenetic changes, particularly DNA methylation. The placenta, a vital organ for fetal and maternal exchange, plays a central role in the onset of PE. Increasing evidence suggests a strong association between DNA methylation, placental function, and the development of PE. This review focuses on the impact of DNA methylation on placental development and its contribution to PE pathophysiology. It aims to clarify the epigenetic processes essential for normal placental development and explore potential epigenetic biomarkers and therapeutic targets for PE. Such insights could lead to the development of novel preventive and therapeutic strategies for this condition.
子痫前期（PE）是一种常见且多方面的妊娠疾病，其特征为高血压、水肿、蛋白尿和全身器官功能障碍。它仍然是妊娠并发症的主要原因之一，但其确切起源和病理生理机制尚未完全明确。目前，唯一确定的治疗方法是分娩，通常需要提前终止妊娠，这会增加新生儿和孕产妇的发病率和死亡率，尤其是在重症病例中。这凸显了进一步研究以阐明其潜在机制并开发针对性干预措施的迫切需求。子痫前期被认为是由多种因素共同作用导致的，包括炎性细胞因子、滋养细胞功能障碍和环境影响，这些因素可能引发表观遗传变化，特别是DNA甲基化。胎盘是胎儿与母体进行物质交换的重要器官，在子痫前期的发病过程中起着核心作用。越来越多的证据表明DNA甲基化、胎盘功能与子痫前期的发生发展之间存在密切关联。本综述聚焦于DNA甲基化对胎盘发育的影响及其在子痫前期病理生理学中的作用。旨在阐明正常胎盘发育所必需的表观遗传过程，并探索子痫前期潜在的表观遗传生物标志物和治疗靶点。这些见解可能会促成针对该病症的新型预防和治疗策略的开发。
