期刊
CELL HOST & MICROBE
卷 13, 期 2, 页码 215-226出版社
CELL PRESS
DOI: 10.1016/j.chom.2013.01.010
关键词
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资金
- Global Alliance to Prevent Preterm Birth and Still birth and Grand Challenges in Global Health: Preventing Preterm Birth Initiative [12003]
- Canadian Institutes of Health Research (CIHR) [MOP-115160, 13721]
- Canada Research Chair
- Doctoral Research Award
- Genome Canada through the Ontario Genomics Institute
- MITACS Elevate Postdoctoral Fellowship
- Wellcome Trust
Placental malaria (PM) is a major cause of fetal growth restriction, yet the underlying mechanism is unclear. Complement C5a and C5a receptor levels are increased with PM. C5a is implicated in fetal growth restriction in non-infection-based animal models. In a case-control study of 492 pregnant Malawian women, we find that elevated C5a levels are associated with an increased risk of delivering a small-for-gestational-age infant. C5a was significantly increased in PM and was negatively correlated with the angiogenic factor angiopoietin-1 and positively correlated with angiopoietin-2, soluble endoglin, and vascular endothelial growth factor. Genetic or pharmacological blockade of C5a or its receptor in a mouse model of PM resulted in greater fetoplacental vessel development, reduced placental vascular resistance, and improved fetal growth and survival. These data suggest that C5a drives fetal growth restriction in PM through dysregulation of angiogenic factors essential for placental vascular remodeling resulting in placental vascular insufficiency.
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