Fetal Origin of Hypercholesterolemia

Numerous studies have demonstrated the existence of fetal developmental origin of adult hypercholesterolemia. However, a comprehensive theory underlying the pathogenesis of fetal-originated hypercholesterolemia is still lacking. Recent studies have revealed that an adverse intrauterine environment, such as xenobiotic exposure, can induce the fetus to become overexposed to maternal-originated glucocorticoids by opening the placental glucocorticoid barrier. This overexposure can directly affect liver cholesterol metabolic function in utero or indirectly through maternal-originated glucocorticoids, resulting in offspring susceptibility to hypercholesterolemia after birth. Epigenetic modifications also participate in regulating the intrauterine programming mechanism of fetal-originated hypercholesterolemia. This chapter summarizes the research progress of fetal-originated hypercholesterolemia and its intrauterine programming mechanism, providing a theoretical and experimental foundation for clinical early warning and treatment.