{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T14:36:55Z","timestamp":1773326215571,"version":"3.50.1"},"reference-count":10,"publisher":"Portland Press Ltd.","issue":"3","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2009,2,1]]},"abstract":"<jats:p>Pre-eclampsia, a pregnancy complication characterized by hypertension and proteinuria, is still a major cause of neonatal and maternal mortality, and acute and long-term morbidities for both mother and neonate. There is mounting evidence that an imbalance between angiogenic factors, such as VEGF (vascular endothelial growth factor) or PlGF (placental growth factor), and factors inhibiting angiogenesis, such as sFlt1 (soluble fms-like tyrosine kinase 1) and sEng (soluble endoglin), are closely related to the pathogenesis of pre-eclampsia. In the present issue of Clinical Science, Bills and co-workers report that VEGF165b, an alternative splice variant of the VEGF pre-mRNA, is up-regulated in women with normal pregnancy and that this increase was delayed or diminished in women who developed pre-eclampsia. Thus this protein could serve (alone or in combination with other parameters) as a new marker for risk assessment in terms of pre-eclampsia.<\/jats:p>","DOI":"10.1042\/cs20080598","type":"journal-article","created":{"date-parts":[[2008,11,27]],"date-time":"2008-11-27T12:25:33Z","timestamp":1227788733000},"page":"231-232","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Angiogenic factors and pre-eclampsia: an early marker is needed"],"prefix":"10.1042","volume":"116","author":[{"given":"Holger","family":"Stepan","sequence":"first","affiliation":[{"name":"1Department of Obstetrics, Leipzig University, Liebigstr. 20a, 04103 Leipzig, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2009,1,8]]},"reference":[{"key":"2021113010113783000_B1","doi-asserted-by":"crossref","first-page":"785","DOI":"10.1016\/S0140-6736(05)17987-2","article-title":"Pre-eclampsia","volume":"365","author":"Sibai","year":"2005","journal-title":"Lancet"},{"key":"2021113010113783000_B2","doi-asserted-by":"crossref","first-page":"649","DOI":"10.1172\/JCI17189","article-title":"Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia","volume":"111","author":"Maynard","year":"2003","journal-title":"J. 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