| Literature DB >> 16433827 |
Abstract
In this review, a novel and unifying pathophysiologic mechanism of preeclampsia is presented whereby a minimal excess of placental immune complex production versus removal causes a proinflammatory autoamplification cascade of trophoblast apoptosis/necrosis and oxidative stress, culminating in clinical preeclampsia. This concept immediately leads to a plethora of new and robust therapeutic strategies.Entities:
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Year: 2006 PMID: 16433827 DOI: 10.1111/j.1600-0897.2005.00362.x
Source DB: PubMed Journal: Am J Reprod Immunol ISSN: 1046-7408 Impact factor: 3.886