One of the leading causes for maternal and perinatal morbidity and mortality in pregnancy is preeclampsia. Preeclampsia is defined as an increase in blood pressure (>140/90 mmHg) appearing after 20 weeks of gestation and proteinuria (>300 mg/l) in a previously normotensive woman. It is a major healthcare problem, affecting 5–7% of pregnant women worldwide and mothers and children suffer from an increased long-term cardiovascular risk. Nonetheless, the underlying molecular mechanisms remain unclear, immunological mechanisms and the renin–angiotensin system have been implicated in the development of these pregnancy disorder. Agonistic autoantibodies to the angiotensin II receptor type I (AT1-AA) have been identified in preeclamptic mothers and fetus. This observation unified the two hypothesis he epitope is located on the second extracellular loop of the AT1-receptor. AT1-AA induce signal transduction including the protein kinase C, the mitogen-activated protein pathway and activate the transcription factors NF-kB and AP-1. AT1-AA have been found in various rat models of preeclampsia. These data indicate that the generation of AT1-AA may be secondary to placental ischemia, vascular damage, and enhanced inflammatory response. Passive transfer of AT1-AA to pregnant rodents induce a preeclamptic phenotype and an angiotensin II sensitivity which also appears in the human situation.
The data support the hypothesis that preeclampsia is an autoimmune disease in which key features of the disease result from autoantibody-induced angiotensin receptor activation. This hypothesis has implications regarding preeclampsia screening, diagnosis and therapy. However, future studies are warranted to confirm this hypothesis.
Disclosure of Interest None Declared
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