RESUMEN
Racial disparities exist in the prevalence of preeclampsia (PE), with women of African ancestry suffering the highest rates of morbidity and mortality. Genetic changes may play a role in the preponderance of PE among women of African ancestry. This review discusses 30 genes with variants that have been studied in PE in women of African ancestry. These studies found that a single gene is not responsible for PE susceptibility as 13 genes have been implicated. These genes subserve endothelial, immune, hemodynamic, homeostatic, thrombophilic, oxidative stress, and lipid metabolic pathways. Notably, maternal-fetal gene interactions also contribute to the susceptibility of the disease. For instance, the maternal KIR AA genotype and paternally inherited fetal HLA-C2 genotype confer risk for developing PE. Additionally, genetic changes such as epigenetic modulation of expression of the MTHFR gene through DNA methylation is also associated with the occurrence of PE. In contrast, some genes such as the KIR B centromeric region protect against development of PE in some women. The soluble fms-like tyrosine kinase 1 (sFlt-1) contributes to the development of PE and is a potential novel therapeutic option for targeted gene silencing of anti-angiogenic sFLT-1 gene. Additionally, NOS3 gene is an important target for pharmacogenomics because it is responsible for the production of endothelial nitric oxide. In conclusion, maternal genetic and epigenetic variants confer susceptibility to PE, indicating the need for further studies to develop a screening tool incorporating maternal genetic variants to identify women at high risk for PE and offer them a preventive therapy.