Potential for miRNAs as Biomarkers and Therapeutic Targets in Preeclampsia
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
See related article, pp 721–730
Preeclampsia is a pregnancy-specific disorder with adverse maternal and fetal outcomes that impacts 5% to 7% of all pregnancies in the United States.1 Although the pathogenesis of this disease is not well understood, recent progress has provided potential mechanisms for treating preeclampsia-induced injury. Whether preeclampsia develops before (early onset) or after (late onset) 34 weeks of gestation is important for the cause, severity, and prognosis of the disease. Early-onset preeclampsia is more often associated with intrauterine growth restriction and adverse neonatal and maternal outcomes, whereas late-onset preeclampsia induces less severe outcomes. Although there is limited understanding of the mechanisms leading to early-onset preeclampsia, insufficient invasion of trophoblast cells into spiral arteries coincident with shallow uterine invasion often accompanies the diagnosis. Placental ischemia develops as a result of insufficient vascular remodeling and induces the release of detrimental soluble factors into the maternal circulation, leading to endothelial dysfunction and hypertension.2 Multiple factors contribute to the development of placental syndrome, including immune and inflammatory cytokines, oxidative stress and mitochondrial dysfunction, damage-associated molecular patterns, components of the renin–angiotensin system, genetic and genomic factors, …