Preeclampsia (PE) is a severe pregnancy complication. The exact pathogenesis of PE remains unclear, but it is related to immune, inflammatory, circulatory, and oxidative stress factors. Leptin is a protein involved in these processes and is essential for maintaining a normal pregnancy and healthy fetal growth. Abnormal increases in leptin levels have been observed in the peripheral blood and placenta of patients with PE. Disturbances in leptin can affect the proliferation and hypertrophy of vascular smooth muscle cells, which are important for placentation. Leptin also regulates arterial tension and trophoblast function in pregnant women. In addition, consistently high levels of leptin are linked to hyperactive inflammation and oxidative stress reactions in both patients with PE and animal models. This review focuses on the role of leptin in the pathophysiology of PE and elucidates its potential mechanisms.