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Review
. 2011 Jun 21;123(24):2856-69.
doi: 10.1161/CIRCULATIONAHA.109.853127.

Preeclampsia, a disease of the maternal endothelium: the role of antiangiogenic factors and implications for later cardiovascular disease

Camille E Powe  1 , Richard J Levine, S Ananth Karumanchi
Affiliations
Review

Preeclampsia, a disease of the maternal endothelium: the role of antiangiogenic factors and implications for later cardiovascular disease

Camille E Powe et al. Circulation. .
No abstract available

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Figures

Figure 1
Figure 1. Abnormal Placentation in Preeclampsia
In normal placental development, invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries, transforming them from small-caliber resistance vessels to high-caliber capacitance vessels capable of providing placental perfusion adequate to sustain the growing fetus. During the process of vascular invasion, the cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as “pseudovasculogenesis” or “vascular mimicry” (Upper Panel). In preeclampsia, cytotrophoblasts fail to adopt an invasive endothelial phenotype. Instead, invasion of the spiral arteries is shallow and they remain small caliber, resistance vessels (Lower Panel). Figure reproduced with permission from Lam et al.
Figure 2
Figure 2. sFlt1 and sEng Causes Endothelial Dysfunction by Antagonizing VEGF and TGF-β1 signaling
There is mounting evidence that VEGF and TGF-β1 are required to maintain endothelial health in several tissues including the kidney and perhaps the placenta. During normal pregnancy, vascular homeostasis is maintained by physiological levels of VEGF and TGF-β1 signaling in the vasculature. In preeclampsia, excess placental secretion of sFlt1 and sEng (two endogenous circulating anti-angiogenic proteins) inhibits VEGF and TGF-β1 signaling respectively in the vasculature. This results in endothelial cell dysfunction, including decreased prostacyclin, nitric oxide production and release of procoagulant proteins.
Figure 3
Figure 3. Summary of the pathogenesis of preeclampsia
AT1-AA, immunological factors, oxidative stress and other factors (such as decreased hemoxygenase expression) may cause placental dysfunction which in turn leads to the release of anti-angiogenic factors (such as sFlt1 and sEng) and other inflammatory mediators to induce preeclampsia
Figure 4
Figure 4
Model for pregnancy as a stress test for long term cardiovascular disease. This model suggests that the women who develop preeclampsia (red line) have greater underlying vascular risk. This manifests during pregnancy (two pregnancies are represented) in the form of preeclampsia as well as later in life in the form of hypertension, heart disease, stroke, and other forms of cardiovascular disease. In women without these underlying vascular risk factors (blue line), pregnancy may increase vascular risk slightly, but not enough to lead to preeclampsia. These women have a lower cardiovascular risk both during pregnancy and later in life. Figure adapted from Sattar et al
See this image and copyright information in PMC

References

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