Hematological Markers: Emerging Diagnostic and Therapeutic Targets in Preeclampsia

Preeclampsia is a morbid hypertensive disease with an onset at gt;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.