Abstract
Preeclampsia (PE) remains a leading cause of fetal and maternal mortality. Angiotensin II type 1 receptor autoantibody (AT1-AA) is implicated in the dysregulation of the renin-angiotensin-aldosterone system. A strong relationship between AT1-AA and the occurrence and severity of PE has been confirmed in previous literature. Recent evidences suggested that AT1-AA was responsible for blood pressure elevation, reactive oxygen species synthesis, and inflammatory factors release and engaged in multiple signaling cascades. The inhibition of AT1-AA might be a potential therapeutic target in future days. Here we reviewed the current understanding of AT1-AA, aiming to provide clarity surrounding the role of AT1-AA in PE.
Disclosure statement
No potential conflict of interest was reported by the author(s).