NFĸB and its inhibitors in preeclampsia: mechanisms and potential interventions

Preeclampsia (PE), which affects between 2 and 15% of pregnancies, is one of the most often reported prenatal problems. It is defined as gestational hypertension beyond 20 weeks of pregnancy, along with widespread edema or proteinuria and specific types of organ damage. PE is characterized by increased levels and activation of nuclear factor kappa B (NF-κB) in the mother's blood and placental cells. This factor controls over 400 genes linked to inflammatory, apoptotic, angiogenesis, and cellular responses to hypoxia and oxidative stress. In the final stages of physiological pregnancy, NF-κB levels need to be lowered to favor maternal immunosuppressive events and continue gestation to prevent hypoxia and inflammation, which are advantageous for implantation. Pharmacotherapy is thought to be a potential treatment for PE by downregulating NF-κB activation. NF-κB activity has been discovered to be regulated by several medications used for both prevention and treatment of PE. However, in order to guarantee treatment safety and effectiveness, additional creativity is desperately required. This article provides an overview of the current understanding of the defined function of NF-κB in PE progression. According to their effect on the cellular control of NF-κB pathways, newly proposed compounds for preventing and treating PE have also been emphasized.