Preeclampsia is a hypertensive disorder of pregnancy. It affects 2% to 8% of pregnancies worldwide and causes significant maternal and perinatal morbidity and mortality. Hypertension and proteinuria are the cornerstone of the disease, though systemic organ dysfunction may ensue. The clinical syndrome begins with abnormal placentation with subsequent release of antiangiogenic markers, mediated primarily by soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng). High levels of sFlt-1 and sEng result in endothelial dysfunction, vasoconstriction, and immune dysregulation, which can negatively impact every maternal organ system and the fetus. This review comprehensively examines the pathogenesis of preeclampsia with a specific focus on the mechanisms underlying the clinical features. Delivery is the only definitive treatment. Low-dose aspirin is recommended for prophylaxis in high-risk populations. Other treatment options are limited. Additional research is needed to clarify the pathophysiology, and thus, identify potential therapeutic targets for improved treatment and, ultimately, outcomes of this prevalent disease.