Spiral artery remodeling, which is indispensable for successful pregnancy, is accomplished by endovascular trophoblasts that move upstream along the arterial wall, replace the endothelium, and disrupt the muscular lining. This review outlines the possible factors that could regulate endovascular trophoblast differentiation and invasion. First, high oxygen tension in the spiral artery could initiate endovascular trophoblast invasion. Second, activation of maternal decidual natural killer (dNK) cells could support perivascular invasion of interstitial trophoblasts and consequently could facilitate the endovascular trophoblast invasion. Third, maternal platelets trapped by the endovascular trophoblasts could enhance endovascular trophoblast invasion, which is in part mediated by chemokine CCL5 (C-C motif ligand 5) released from the activated platelets and chemokine receptor CCR1 (C-C chemokine receptor type 1) expressed specifically on the endovascular trophoblasts. The rat, in which trophoblast cells exhibit extensive interstitial and endovascular invasion, could be a suitable model animal for the study of human spiral artery remodeling. Apparently paradoxical results came from the rat study, i.e., exposure to hypoxia or depletion of dNK cells resulted in acceleration of the endovascular trophoblast invasion. This implies the presence of as-yet-undetermined regulator(s) whose effects on endovascular trophoblast invasion surpass the effects of surrounding oxygen tension or maternal dNK cells. In the future, clarification of the molecular differences between human interstitial and endovascular trophoblasts as well as establishment of the pregnant rat model exhibiting shallow endovascular trophoblast invasion and preeclamptic symptoms will contribute to elucidating the mechanism of spiral artery remodeling.

中文翻译：

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血管内滋养细胞和螺旋动脉重塑。

成功怀孕必不可少的螺旋动脉重塑是通过沿血管壁向上游移动，替换内皮并破坏肌肉内膜的血管内滋养细胞实现的。这篇综述概述了可能调节血管内滋养细胞分化和侵袭的可能因素。首先，螺旋动脉中的高氧张力可能引发血管内滋养细胞的侵袭。其次，激活母体蜕膜自然杀伤细胞（dNK）可以支持血管间质滋养细胞的血管周侵袭，因此可以促进血管内滋养细胞的侵袭。第三，母体血小板被血管内滋养细胞捕获可以增强血管内滋养细胞的侵袭，它由活化的血小板释放的趋化因子CCL5（CC基序配体5）和在血管内滋养细胞上特异性表达的趋化因子受体CCR1（CC趋化因子受体1型）介导。滋养层细胞表现出广泛的间质和血管内侵袭的大鼠，可能是研究人类螺旋动脉重塑的合适模型动物。显然矛盾的结果来自大鼠研究，即暴露于缺氧或dNK细胞耗竭导致血管内滋养细胞入侵加速。这意味着存在尚未确定的调节剂，其对血管内滋养层细胞侵袭的影响超过周围的氧气张力或母体dNK细胞的影响。将来，