Preeclampsia is one of the most severe obstetric complications, yet its pathogenesis remains unclear. Decidual natural killer (dNK) cells, the most abundant immune cells at the maternal‐fetal interface, are closely associated with preeclampsia due to abnormalities in their quantity, phenotype, and function. This review summarizes the molecular mechanisms by which dNK cells regulate extravillous trophoblast (EVT) invasion, promote uterine spiral artery remodeling, and maintain immune tolerance. Furthermore, it explores how disruptions in these mechanisms and changes in the decidual microenvironment alter dNK cell properties, driving the progression of preeclampsia. Understanding the mechanisms of dNK cells and identifying potential therapeutic targets may provide new insights for clinical intervention.