Preeclampsia remains a leading cause of maternal and fetal mortality, due to ineffective treatment and diagnostic strategies, compounded by the lack of clarity on the etiology of the disorder. Although several clinical and biological markers of preeclampsia have been evaluated, they have proven to be ineffective in providing a definitive diagnosis during the various stages of the disorder. Exosomes have emerged as ideal biomarkers of pathological states, such as cancer, and have more recently gained interest in pregnancy-related complications, due to their role in cellular communication in normal and complicated pregnancies. This occurs as a result of the specific placenta-derived exosomal molecular cargo, which may be involved in normal pregnancy-associated immunological events, such as the maintenance of maternal–fetal tolerance. This review provides perspectives on placenta-derived exosomes as possible biomarkers for the diagnosis/prognosis of preeclampsia. Using keywords, online databases were searched to identify relevant publications to review the potential use of placenta-derived exosomes as biomarkers of preeclampsia.

Background: Preeclampsia is the leading cause of maternal and fetal mortality due to the inability to diagnose and treat the disorder early in pregnancy. This is attributed to the complex pathophysiology and unknown etiology of the disorder, which is modulated by several known and unknown factors. Exosomes have recently been implicated as possible mediators of the pathogenesis of preeclampsia, with, however, no evidence linking these nanovesicles to the pathophysiology of preeclampsia and its subtypes. Methods: To better understand the pathophysiological role of exosomes in preeclampsia, we have analyzed the exosomal microRNA in early and late onset preeclamptic women in comparison to their gestationally matched normotensive controls using Digital Direct Detection (NanoString Technologies). Results: For the first time, distinct exosomal microRNA signatures in early and late onset preeclampsia have been identified. Moreover, these signatures indicate that exosomes are involved in key pathological features associated with preeclampsia and differentiate between the subtypes. Conclusion: This study forms the basis for the diagnostic and functional validation of the identified signatures as biomarkers of preeclampsia and its subtypes.

Salt-sensitive hypertension can be caused through abnormalities related to sodium and body fluid homeostasis; renin-angiotensin-aldosterone (RAAS) plays a key role in this regard. The molecular basis of the purported antihypertensive benefits of some plant-derived compounds such as quercetin is still lacking. To this end, we investigated RAAS in the Dahl salt-sensitive rat model with emphasis on the kidney. Eighteen rats were treated with captopril (CAP), quercetin (QUE), and dimethyl sulfoxide (controls) over a 4-week period. CAP and QUE lowered systolic blood pressure significantly in comparison to day 0 (baseline values). These findings were in keeping with their increased urinary output, increased sodium output, decreased aldosterone and decreased AT1a mRNA. QUE did not differ significantly from controls with regards to aldosterone levels. QUE was effective in lowering blood pressure in this model of hypertension, probably because of a modulation of renal function.