The results from the rodent studies suggest two important conclusions that are consistent with the human disease. First, pre-eclampsia can be initiated by several different means. These data are consistent with recent human genetic studies that rule out simple genetic mechanisms (Arngrimsson et al., 1995; Lachmeijer et al., 2001, 2002; Roberts and Cooper, 2001; Treloar et al., 2001), and actually implicate more than one locus (Lachmeijer etal., 2002; Roberts and Cooper, 2001). Collectively these studies should give pause to investigators who may be trying to find the ''one cause'' of pre-eclampsia. Second, either a strict maternal susceptibility to hypertension or a feto-placental defect is sufficient to cause pre-eclamp-sia. This idea is supported by a study of pregnancy outcomes in twin sisters that indicated that pre-eclampsia is unlikely to have a strictly maternal basis (Treloar et al., 2001). These studies highlight the need to classify the disease into different types (e.g. maternal versus feto-placental origin) when trying to assign etiologies.
While the rodent models have been very useful to date in defining the maternal and feto-placental contributions to pre-eclampsia, and in highlighting specific factors that precipitate the disease, these models should prove equally useful in outlining the progression of the disease. It is interesting that the events of later development that take the last 8 months of gestation in humans occur in only the last 9 days in mice, and yet this short time is sufficient for the clinical signs to develop. This is a huge theoretical advantage when trying to identify feto-placental factors that contribute to normal cardiovascular adaptations to pregnancy and to disease, because it considerably narrows the window during which to look. It should therefore allow investigators to more likely identify markers of disease onset rather than simply the ongoing disease itself.
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