Preeclampsia is a morbid hypertensive disease with an onset at >20 weeks of
gestation. It has a global incidence of 2-10%, contributing to a large share of fetal and
maternal mortality. Pathophysiology of the disease is multifaceted with the
involvement of immunological, genetic, and inflammatory factors. Faulty placentation
with abnormal angiogenesis and apoptosis is pivotal with subsequent hypoxia and
oxidative stress leading to widespread systemic inflammation. For years placenta has
been the center of research to elucidate the pathogenesis and treatment strategies of
preeclampsia. Recently numerous circulating immunological, genetic, and
inflammatory markers have emerged as a focus of interest and intrigued the researchers
to mark their contribution to the pathogenesis of the disease. Elevated levels of proinflammatory
factors like Tumor Necrosis Factor-alpha (TNF-α), soluble Endoglin
(sENG), soluble Flt-1 (sFlt-1), Nuclear factor kappa B (NFκB), Interleukin 6 (IL-6),
Interleukin 8 (IL-8), and Angiotensin II, etc. have been labeled as contributors to the
maternal endothelial dysfunction, a hallmark of preeclampsia. MicroRNAs (the
emerging field of research) belong to the noncoding RNAs that can modulate the
expression of these inflammatory markers. Recent reports on the differential profile of
various microRNAs in preeclampsia have focused on using these as diagnostic and
therapeutic targets. Modifying the expression levels of different genes involved in
inflammation, angiogenesis, and apoptosis can change the clinical picture and
prognosis of the disease.
Keywords: Angiogenesis, Apoptosis, Endothelial dysfunction, Inflammation, Inter Leukins, MiRNAs, Oxidative stress, Preeclampsia, sEndoglin, sFlt-1, Syncytiotrophoblasts, TNF-α.
