Preeclampsia is a complex hypertensive disorder of pregnancy characterized by systemic inflammation, endothelial dysfunction, and placental insufficiency, contributing significantly to maternal and fetal morbidity. Recent evidence underscores the role of adipokines—bioactive molecules secreted by adipose tissue and the placenta—in the pathophysiology of preeclampsia. This review explores the dysregulated expression and function of key adipokines, such as leptin, adiponectin, resistin, chemerin, visfatin, and omentin in preeclamptic pregnancies. Pro-inflammatory adipokines (leptin, resistin, chemerin, and visfatin) are consistently upregulated, amplifying inflammatory signaling (e.g., JAK/STAT, TLR4/NF-κB) and promoting endothelial dysfunction. Conversely, anti-inflammatory adipokines (adiponectin and omentin) are markedly downregulated, weakening vasoprotective and metabolic regulatory pathways. These alterations are closely linked to gene expression changes in placental and adipose tissues under hypoxic and inflammatory conditions, forming a feed-forward loop of vascular injury. Furthermore, adipokines are emerging as promising biomarkers for early diagnosis and risk stratification in preeclampsia, with clinical studies correlating their plasma levels to disease onset and severity. Therapeutic modulation of adipokine signaling pathways offers a novel approach to restoring metabolic-vascular homeostasis in high-risk pregnancies. By integrating current molecular insights, this review provides a comprehensive framework for understanding adipokine-mediated mechanisms in preeclampsia and highlights their potential in improving prediction, prevention, and management strategies.