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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tong S. | en |
dc.contributor.author | Kaitu'u-Lino T.J. | en |
dc.contributor.author | Palmer, Kirsten R. | en |
dc.date.accessioned | 2021-05-14T13:12:46Z | en |
dc.date.available | 2021-05-14T13:12:46Z | en |
dc.date.copyright | 2017 | en |
dc.date.created | 20170703 | en |
dc.date.issued | 2017-07-03 | en |
dc.identifier.citation | Molecular Human Reproduction. 23 (2) (pp 69-78), 2017. Date of Publication: 06 Feb 2017. | en |
dc.identifier.issn | 1360-9947 | en |
dc.identifier.uri | https://repository.monashhealth.org/monashhealthjspui/handle/1/38703 | en |
dc.description.abstract | Pre-eclampsia is a common obstetric complication globally responsible for a significant burden of maternal and perinatal morbidity and mortality. Central to its pathophysiology is the anti-angiogenic protein, soluble fms-like tyrosine kinase-1 (sFLT-1). sFLT-1 is released from a range of tissues into the circulation, where it antagonizes the activity of vascular endothelial growth factor and placental growth factor leading to endothelial dysfunction. It is this widespread endothelial dysfunction that produces the clinical features of preeclampsia including hypertension and proteinuria. There are multiple splice variants of sFLT-1. One, known as sFLT-1 e15a, evolved quite recently and is only present in humans and higher order primates. This sFLT-1 variant is also the main sFLT-1 secreted from the placenta. Recent work has shown that sFLT-1 e15a is significantly elevated in the placenta and circulation of women with pre-eclampsia. It is also biologically active, capable of causing endothelial dysfunction and the end-organ dysfunction seen in pre-eclampsia. Indeed, the over-expression of sFLT-1 e15a in mice recapitulates the pre-eclamptic phenotype in pregnancy. Therefore, here we propose that sFLT-1 e15a may be the sFLT-1 variant primarily responsible for pre-eclampsia, a uniquely human disease. Furthermore, this placental-specific sFLT-1 variant provides promise for use as an accurate biomarker in the prediction or diagnosis of pre-eclampsia.Copyright © The Author 2016. | en |
dc.language | English | en |
dc.language | en | en |
dc.publisher | Oxford University Press (E-mail: jnl.info@oup.co.uk) | en |
dc.relation.ispartof | Molecular Human Reproduction | en |
dc.title | Placental-specific sFLT-1: Role in pre-eclamptic pathophysiology and its translational possibilities for clinical prediction and diagnosis. | en |
dc.type | Review | en |
dc.type.studyortrial | Review article (e.g. literature review, narrative review) | - |
dc.identifier.doi | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1093/molehr/gaw077 | en |
dc.publisher.place | United Kingdom | en |
dc.identifier.pubmedid | 27986932 [http://www.ncbi.nlm.nih.gov/pubmed/?term=27986932] | en |
dc.identifier.source | 616982866 | en |
dc.identifier.institution | (Palmer) Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia (Palmer, Tong, Kaitu'u-Lino) Translational Obstetric Group, University of Melbourne, Mercy Hospital for Women, 163 Studley Rd, Heidelberg, VIC 3084, Australia | en |
dc.description.address | K.R. Palmer, Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia. E-mail: kirsten.palmer@monash.edu | en |
dc.description.publicationstatus | Embase | en |
dc.rights.statement | Copyright 2017 Elsevier B.V., All rights reserved. | en |
dc.subect.keywords | Anti-angiogenic factors Hypoxia Placenta Pre-eclampsia sFLT-1 Splice variant VEGF | en |
dc.identifier.authoremail | Palmer K.R.; kirsten.palmer@monash.edu | en |
item.cerifentitytype | Publications | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | none | - |
item.openairetype | Review | - |
crisitem.author.dept | Obstetrics and Gynaecology (Monash Women's) | - |
Appears in Collections: | Articles |
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