title: Advances in the pathophysiology of pre-eclampsia and related podocyte injury.
abstract: Pre-eclampsia is a pregnancy-specific hypertensive disorder that may lead to serious maternal and fetal complications. It is a multisystem disease that is commonly, but not always, accompanied by proteinuria. Its cause(s) remain unknown, and delivery remains the only definitive treatment. It is increasingly recognized that many pathophysiological processes contribute to this syndrome, with different signaling pathways converging at the point of systemic endothelial dysfunction, hypertension, and proteinuria. Different animal models of pre-eclampsia have proven utility for specific aspects of pre-eclampsia research, and offer insights into pathophysiology and treatment possibilities. Therapeutic interventions that specifically target these pathways may optimize pre-eclampsia management and may improve fetal and maternal outcomes. In addition, recent findings regarding placental, endothelial, and podocyte pathophysiology in pre-eclampsia provide unique and exciting possibilities for improved diagnostic accuracy. Emerging evidence suggests that testing for urinary podocytes or their markers may facilitate the prediction and diagnosis of pre-eclampsia. In this review, we explore recent research regarding placental, endothelial, and podocyte pathophysiology. We further discuss new signaling and genetic pathways that may contribute to pre-eclampsia pathophysiology, emerging screening and diagnostic strategies, and potential targeted interventions.
authors.affiliation: Division of Nephrology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
authors.forename: Iasmina M
authors.initials: IM
authors.lastname: Craici
authors.affiliation: Division of Nephrology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Wagner
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
authors.forename: Tracey L
authors.initials: TL
authors.lastname: Weissgerber
authors.affiliation: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
authors.forename: Joseph P
authors.initials: JP
authors.lastname: Grande
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
authors.forename: Vesna D
authors.initials: VD
authors.lastname: Garovic
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D002248:Carbon Monoxide / Q000502:physiology; D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology; D019332:Endothelin-1 / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D044127:Epigenesis, Genetic; D005260:Female; D006419:Heme Oxygenase (Decyclizing) / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D018919:Neovascularization, Physiologic; D009569:Nitric Oxide / Q000502:physiology; D010920:Placenta / Q000098:blood supply / Q000503:physiopathology; D010929:Placentation / Q000502:physiology; D050199:Podocytes / Q000502:physiology*; D011225:Pre-Eclampsia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D011247:Pregnancy; D051880:Receptors, Notch / Q000235:genetics / Q000502:physiology; D051436:Renal Insufficiency, Chronic / Q000209:etiology; D015398:Signal Transduction
chemical_list: D002352:Carrier Proteins; D019332:Endothelin-1; D051880:Receptors, Notch; C500784:STOX1 protein, human; D009569:Nitric Oxide; D002248:Carbon Monoxide; D006419:Heme Oxygenase (Decyclizing)