Preeclampsia is the leading cause of death and morbidity worldwide for the mother and fetus
during pregnancy. Preeclampsia does not only affect the mother and the baby during pregnancy,
but can also have long-term effects, such as the increased risk of hypertension and cardiovascular disease
on the offspring and the postpartum mother later in life. The exact cause of preeclampsia is unknown,
but women with preeclampsia have elevated concentrations of agonistic autoantibodies against
the angiotensin II type 1 receptor (AT1-AA). These AT1-AA’s through multiple studies have shown to
play a significant role in the pathology and possible genesis of preeclampsia. This review will discuss
the discovery of AT1-AAs and the role of AT1-AAs in the pathophysiology of preeclampsia. This review
will also discuss future therapeutic approaches towards the AT1-AA to prevent adverse pregnancy
outcomes. Furthermore, we will examine the relationship between AT1-AA induced hypertension
associated with increased oxidative stress, antiangiogenic factors (such as soluble fms-related tyrosine
kinase-1 (sFlt-1), endothelin-1 (ET-1), inflammation, endothelial dysfunction, and reduced renal
function. Understanding the pathological role of AT1-AAs in hypertensive pregnancies is important as
we search for novel therapies to manage preeclampsia.
Keywords: Preeclampsia, angiotensin II type 1 receptor autoantibody (AT1-AA), oxidative stress, renal function, endothelin.
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