Pathogenesis of uteroplacental acute atherosis: An update on current research

Uteroplacental acute atherosis is a type of arterial vascular disease that affects the placenta during pregnancy and predominates in the maternal spiral arteries in the decidua basalis layer of the pregnant uterus. This condition is characterized by fibrin-like necrosis of the blood vessel walls, the accumulation of macrophages containing fat (foam cells), and the infiltration of macrophages around blood vessels. Uteroplacental acute atherosis is rare in normal pregnancy but occurs more frequently in patients with pregnancy complications, including preeclampsia, spontaneous preterm labor, preterm prelabor rupture of membranes, mid-trimester spontaneous abortion, fetal death, and small-for-gestational age. It is believed that the mechanisms underlying the development of uteroplacental acute atherosis are related to the incomplete physiological transformation of spiral arteries, placental inflammation, abnormal lipid metabolism, and oxidative stress. In this review, we describe the pathogenesis of uteroplacental acute atherosis to provide reference guidelines for the future prevention and treatment of uteroplacental acute atherosclerotic disease.