作者: Aernout Luttun , Peter Carmeliet
DOI: 10.1172/JCI18015
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摘要: The occurrence of seizures (eclampsia, from the Greek “eklampsis,” sudden flashing) has been a long-known and feared complication pregnancy, often killing both mother child. Preeclampsia, or condition preceding full-blown eclampsia, affects up to 5% pregnant women is diagnosed by onset hypertension proteinuria in second trimester (1). Preeclampsia may eventually progress glomerular malfunction, thrombocytopenia, liver brain edema, associated life-threatening (2) (Figure (Figure1).1). sometimes termed “disease theories,” as several models for its pathogenesis have proposed. But, today, no satisfactory unifying hypothesis emerged restricted preeclampsia humans primates lack suitable animal model hampered understanding (3). In this issue JCI, S.E. Maynard et al. (4) report novel insight that circulating levels two angiogenic growth factors, VEGF placental factor (PlGF), play more important role than previously believed. particular, authors propose that, with preeclampsia, placenta produces elevated soluble fms-like tyrosine kinase 1 (sFlt1) receptor, which captures free PlGF. As result, normal vasculature kidney, brain, lungs, other organs deprived essential survival maintenance signals becomes dysfunctional show their rodent model, lead development renal disease, reminiscent humans. another study issue, V. Eremina (5) provide additional evidence critical disease during preeclampsia. These demonstrate mice lacking one allele podocytes develop typical pathology found studies therefore shed unprecedented light on offer therapeutic opportunities disease. Figure 1 Hypothesis sFlt1 (a) During uterine spiral arteries are infiltrated remodeled endovascular invasive trophoblasts, thereby increasing blood flow significantly order meet oxygen ...