先兆子痫,怀孕的严重并发症,涉及复杂的分子和细胞机制。胎儿微嵌合,胎儿细胞在母体组织和循环中存在,在子痫前期两阶段模型中,胎盘功能障碍与母体并发症之间的机制联系。激素,补语,细胞因子在病理生理学中起关键作用,影响免疫反应,动脉重塑,和内皮功能。此外,可溶性HLA-G,参与母胎免疫耐受,在先兆子痫中减少。缺氧诱导因子1-α(Hif-α)失调会导致胎盘异常和子痫前期样症状。基质金属蛋白酶(MMPs)的变化,内皮素(ET),趋化因子,和细胞因子有助于有缺陷的滋养层侵入,内皮功能障碍,和炎症。子痫前期的遗传复杂性包括circRNAs,miRNA,和lncRNAs。CircRNA_06354通过经由hsa-miR-92a-3p/VEGF-A途径影响滋养层侵袭而与早发型先兆子痫相关。C19MC的失调,特别是miR-519d和miR-517-5p,影响滋养细胞功能。此外,lncRNAs,如IGFBP1和EGFR-AS1,以及蛋白质编码基因,影响滋养细胞调节和血管生成,影响先兆子痫和胎儿生长。除了CD31+细胞的畸变,其他潜在的生物标志物,如MMP,可溶性HLA-G,和hCG有望预测先兆子痫及其并发症。针对过氧化物酶体PPAR-γ和内皮素受体等因素的治疗性干预显示出减轻先兆子痫相关并发症的潜力。总之,子痫前期是一种病因和发病机制复杂的疾病。胎儿微嵌合,荷尔蒙,补语,和细胞因子有助于胎盘和内皮功能障碍与炎症。识别新的生物标志物和治疗靶点为早期诊断和有效管理提供了希望。最终降低孕产妇和胎儿的发病率和死亡率。然而,需要进一步的研究将这些发现转化为临床实践,并提高高危女性的结局.
Preeclampsia, a serious complication of pregnancy, involves intricate molecular and cellular mechanisms. Fetal microchimerism, where fetal cells persist within maternal tissues and in circulation, acts as a mechanistic link between placental dysfunction and maternal complications in the two-stage model of preeclampsia. Hormones, complements, and cytokines play pivotal roles in the pathophysiology, influencing immune responses, arterial remodeling, and endothelial function. Also, soluble HLA-G, involved in maternal-fetal immune tolerance, is reduced in preeclampsia. Hypoxia-inducible factor 1-alpha (Hif-α) dysregulation leads to placental abnormalities and preeclampsia-like symptoms. Alterations in matrix metalloproteinases (MMPs), endothelins (ETs), chemokines, and cytokines contribute to defective trophoblast invasion, endothelial dysfunction, and inflammation. Preeclampsia\'s genetic complexity includes circRNAs, miRNAs, and lncRNAs. CircRNA_06354 is linked to early-onset preeclampsia by influencing trophoblast invasion via the hsa-miR-92a-3p/VEGF-A pathway. The dysregulation of C19MC, especially miR-519d and miR-517-5p, affects trophoblast function. Additionally, lncRNAs like IGFBP1 and EGFR-AS1, along with protein-coding genes, impact trophoblast regulation and angiogenesis, influencing both preeclampsia and fetal growth. Besides aberrations in CD31+ cells, other potential biomarkers such as MMPs, soluble HLA-G, and hCG hold promise for predicting preeclampsia and its complications. Therapeutic interventions targeting factors such as peroxisome PPAR-γ and endothelin receptors show potential in mitigating preeclampsia-related complications. In conclusion, preeclampsia is a complex disorder with a multifactorial etiology and pathogenesis. Fetal microchimerism, hormones, complements, and cytokines contribute to placental and endothelial dysfunction with inflammation. Identifying novel biomarkers and therapeutic targets offers promise for early diagnosis and effective management, ultimately reducing maternal and fetal morbidity and mortality. However, further research is warranted to translate these findings into clinical practice and enhance outcomes for at-risk women.