Altered Expression of Energy Metabolism-Related Genes in Placental Trophoblast Cells in Preeclampsia.

Abstract

Preeclampsia (PE) is a pregnancy-specific hypertensive disorder characterized by new-onset hypertension after 20 weeks of gestation, with or without proteinuria, frequently accompanied by systemic arteriolar spasm and dysfunction or injury of multiple organs, including the liver, kidneys, and placenta. This study examined changes in glycolysis- and mitochondria-related gene expression in placental trophoblast cells in PE, aiming to elucidate the role of disrupted energy metabolism in its pathogenesis. A total of 86 pregnant women with singleton pregnancies who received routine prenatal care at the Affiliated Hospital of Hebei University between December 2023 and October 2024 and delivered via cesarean section were enrolled. Among them, 30 patients diagnosed with PE were included in the PE group, and 56 normotensive pregnant individuals were assigned to the control group. General clinical data were collected. The mRNA and protein expression levels of HK2, PKM2, silent information regulator two 1 (SIRT1), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) in placental tissue were measured using real-time quantitative polymerase chain reaction and western blot (WB) analysis. There were no statistically significant differences in maternal age at delivery, body mass index, triglycerides, total cholesterol, or high-density lipoprotein cholesterol between groups (p > 0.5). Significant differences were observed in low-density lipoprotein cholesterol, neonatal birth weight, and 1-minute and 5-minute Apgar scores (p < 0.05). Expression levels of HK2, PKM2, and PGC-1alpha were significantly elevated in placental tissue from the PE group compared to the control group (p < 0.01), while SIRT1 expression was significantly reduced (p < 0.05). Placental tissue from patients with PE demonstrated upregulation of HK2, PKM2, and PGC-1alpha, and downregulation of SIRT1. Dysregulated expression of genes and proteins involved in energy metabolism may contribute to the pathogenesis of PE through impaired trophoblast function.