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Ovarian cancer is one of the most common malignant tumors in the female reproductive system. Because of its insidious onset, most patients are already in advanced stage when they have symptoms, and are prone to metastasis and recurrence. The mortality rate of ovarian cancer ranks first among gynecological malignant tumors. Therefore, it is very important to further explore the mechanism of ovarian cancer and find potential therapeutic targets. Angiotensin Ⅱ (Ang Ⅱ) is the most bioactive factor in renin-angiotensin system (RAS), mainly involved in the regulation of metabolism of the body′s blood pressure and salt water. At present, some studies found that it combined with the angiotensin type 1 receptor (AT1R) to activated related pathways and that is closely related to the process of the occurrence and development of ovarian cancer and metastasis. And AT1R antagonists angiotensin receptor blocker (ARB) can selectively bind to AT1R blocking Ang Ⅱ - AT1R pathways, thereby blocking or inhibit Ang Ⅱ role in ovarian cancer. Further study on the mechanism of Ang Ⅱ and its type 1 receptor antagonist in ovarian cancer may provide evidence for new therapeutic targets for ovarian cancer. [ABSTRACT FROM AUTHOR]

Pre-eclampsia is a pregnancy-specific disease and a leading cause of maternal and perinatal death. Until now, no hypothesis can fully explain the pathological changes of pre-eclampsia, which is characterized by early placental trophoblast infiltration and decreased spiral artery remodeling. ACVR2A (activin A receptor type 2A), a member of the transforming growth factor β (TGF-β) receptor family, is considered as an important regulator of reproductive function, especially in the process of decidualization, trophoblast cell infiltration and placental formation. Recent studies have shown that activin A and its receptor play an important regulatory role in the occurrence and development of pre-eclampsia. This paper reviews the relationship between ACVR2A and pre-eclampsia, aiming to provide a new theoretical basis for the pathogenesis, early diagnosis and treatment of pre-eclampsia. [ABSTRACT FROM AUTHOR]

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