<![CDATA[Preeclampsia is one of the most serious complications of pregnancy, contributing significantly to maternal and perinatal morbidity and mortality worldwide. Despite extensive research, the precise molecular mechanisms underlying its pathogenesis remain incompletely understood. This study aims to: (1) analyze the mechanisms of systemic inflammation underlying preeclampsia pathogenesis based on current scientific evidence; (2) examine the role of endothelial dysfunction in the progression and clinical manifestations of preeclampsia; and (3) identify the molecular interactions between inflammatory pathways and endothelial dysfunction as a basis for developing diagnostic biomarkers and therapeutic targets. This study employed a qualitative library research method through a systematic search of PubMed, Google Scholar, and ScienceDirect databases, covering publications from 2022 to 2025. Ten relevant articles were selected based on predefined inclusion and exclusion criteria. The findings reveal that impaired maternal immune tolerance, characterized by reduced regulatory T cells and elevated Th17 differentiation, together with angiogenic imbalance involving increased sFlt-1 and decreased PlGF and VEGF, synergistically drive systemic vascular endothelial damage. Placental mitochondrial dysfunction further amplifies this pathological cycle through excessive reactive oxygen species production. Biomarkers such as LDH, sFlt-1:PlGF ratio, and small RNAs including miRNA-210 demonstrate significant potential for early prediction and severity assessment of preeclampsia. These findings underscore the importance of integrating inflammatory and endothelial markers into a comprehensive diagnostic framework to improve early detection and clinical management of preeclampsia.]]>
