Abstract

Preeclampsia (PE) is a leading cause of maternal and neonatal morbidity and mortality worldwide. Defects in trophoblast invasion, differentiation of extravillous trophoblasts and spiral artery remodeling are key factors in PE development. Currently there are no predictive biomarkers clinically available for PE. Recent technological advancements empowered transcriptome exploration and led to the discovery of numerous non-coding RNA species of which microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are the most investigated. They are implicated in the regulation of numerous cellular functions, and as such are being extensively explored as potential biomarkers for various diseases. Altered expression of numerous lncRNAs and miRNAs in placenta has been related to pathophysiological processes that occur in preeclampsia. In the following text we offer summary of the latest knowledge of the molecular mechanism by which lnRNAs and miRNAs (focusing on the chromosome 19 miRNA cluster (C19MC)) contribute to pathophysiology of PE development and their potential utility as biomarkers of PE, with special focus on sample selection and techniques for the quantification of lncRNAs and miRNAs in maternal circulation.

Highlights

  • Published: 30 September 2021Hypertensive pregnancy complications, including preeclampsia (PE), are one of the most common direct causes of maternal and fetal morbidity and mortality [1]

  • The aim of this review is to summarize the latest knowledge of the molecular mechanisms by which miRNAs (focusing on the chromosome 19 miRNA cluster (C19MC)) and lnRNAs contribute to pathophysiology of PE and to review the latest evidence of their potential utility as biomarkers of PE

  • PE is characterized by extensive dysfunction of the placenta, caused by dysregulation of trophoblast differentiation, invasion and remodeling of the spiral arteries [4,5,6]

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Summary

Introduction

Hypertensive pregnancy complications, including preeclampsia (PE), are one of the most common direct causes of maternal and fetal morbidity and mortality [1]. The LO syndrome is thought to be a disorder predisposed by specific maternal risk factors, such as obesity, diabetes, or chronic hypertension [7,8,9], where limited blood flow between the chorionic villi during placental maturation may lead to placental hypoxia [9]. In both cases, resulting hypoxia and ischemia/reperfusion lead to an increased production of humoral factors from trophoblast cells together with the sequestration of the particles from the surface of the injured syncytium of the human placenta, and their subsequent release into the uteroplacental circulation [10]. The aim of this review is to summarize the latest knowledge of the molecular mechanisms by which miRNAs (focusing on the chromosome 19 miRNA cluster (C19MC)) and lnRNAs contribute to pathophysiology of PE and to review the latest evidence of their potential utility as biomarkers of PE

MicroRNAs
Placental MiRNAs
Placenta Derived Extracellular MiRNAs and Immunomodulation
Circulating MiRNAs as Biomarkers of PE
Preanalytics and Technology
Long Non-Coding RNAs
LncRNAs in PE
Circulating LncRNAs in PE
Conclusions
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