Abstract
In this study, we explored the epigenetic basis of preeclampsia, focusing on hypermethylation of the RASSF1A gene promoter - a topic of growing interest in the field of placental pathology and maternal health. While numerous studies have attempted to unravel the mystery of the etiology of preeclampsia, its pathogenesis remains elusive, challenging the development of precise diagnostic tools and therapeutic approaches. Our study, conducted ethically, documents a comprehensive examination of RASSF1A expression, utilizing advanced methods such as real-time PCR, immunohistochemistry, and immunofluorescence staining to quantify methylation and its functional consequences. The study revealed a profound association between RASSF1A promoter hypermethylation and clinical markers of preeclampsia, including hypertension, proteinuria, and reduced neonatal birth weight. Cell models that replicate the hypoxic conditions encountered in preeclampsia reinforced the link between hypoxia and epigenetic changes in RASSF1A, providing insights into the potential reversibility of gene silencing. This study advances the understanding of the role of RASSF1A in preeclampsia and its potential as a biomarker and epigenetic therapeutic target. Our findings encompass the clinical significance of RASSF1A hypermethylation and suggest a promising trajectory for the use of epigenetic modulation in the management of preeclampsia.