The pathophysiology of preeclampsia involves altered levels of angiogenic factors promoted by hypoxia and autoantibody-mediated mechanisms

dc.contributor.authorLaresgoiti-Servitje, Estibalitzen
dc.contributor.authorGomez-Lopez, Nardhy Yadiraen
dc.contributor.schoolSchool of Paediatrics and Reproductive Health : Obstetrics and Gynaecologyen
dc.date.issued2012en
dc.descriptionExtent: 7p.en
dc.description.abstractPre-eclampsia is a syndrome characterized by inadequate placentation, which is due to deficient trophoblastic invasion of the uterine spiral arteries. This deficiency can lead to placental hypoxia, secretion of proinflammatory cytokines, and release of angiogenic and antiangiogenic factors. Hypoxic conditions in the placenta can promote oxidative stress and the production of angiogenic factors that are antagonized by soluble receptors, which are also elevated in this syndrome. In addition to these factors, the development of hypertension in women with pre-eclampsia may be associated with the renin-angiotensin system and endothelial dysfunction. The presence of antiangiotensin II type 1 receptor autoantibodies is relevant in pre-eclampsia because it has been related to the secretion of antiangiogenic factors through cytokine pathways, indicating that autoimmune mechanisms may participate in the pathophysiology of this syndrome.en
dc.description.statementofresponsibilityEstibalitz Laresgoiti-Servitje and Nardhy Gomez-Lopezen
dc.identifier.citationBiology of Reproduction, 2012; 87(2):36en
dc.identifier.doi10.1095/biolreprod.112.099861en
dc.identifier.issn0006-3363en
dc.identifier.urihttp://hdl.handle.net/2440/74505
dc.language.isoenen
dc.publisherSoc Study Reproductionen
dc.rights© 2012 by the Society for the Study of Reproduction, Inc.en
dc.subjectAT1-AA; angiogenic factor; angiotensin II; angiotensin II type 1 receptor autoantibodies; hypoxia; preeclampsia; reninangiotensin systemen
dc.titleThe pathophysiology of preeclampsia involves altered levels of angiogenic factors promoted by hypoxia and autoantibody-mediated mechanismsen
dc.typeJournal articleen

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