Novel insights into molecular mechanisms of abruption-induced preterm birth.
Novel insights into molecular mechanisms of abruption-induced preterm birth.
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DOI：
10.1017/s1462399410001675
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发表时间：
2010-11-01
影响因子：
6.2
通讯作者：
Lockwood CJ
中科院分区：
文献类型：
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作者：
Buhimschi CS;Schatz F;Krikun G;Buhimschi IA;Lockwood CJ
超过 12% 的分娩因早产 (PTB) 而变得复杂。尽管进行了大量研究，但大多数 PTB 病例的病因学仍然难以捉摸。 PTB 的两个主要前因，即羊膜内感染和蜕膜出血（早产），尽管具有共同的分子和细胞途径，但可能表现出不同的人口和遗传倾向。高通量、高维技术的使用揭示了凝血和炎症途径之间的大量串扰。组织因子、凝血酶和细胞因子是这种串扰的关键介质。破裂与蜕膜细胞表达的组织因子产生的过量凝血酶有关。虽然凝血酶是凝血级联的主要介质，但它也可以通过增强基质金属蛋白酶和中性粒细胞趋化和激活趋化因子的表达来促进炎症相关的 PTB。在这里，我们对胎盘早剥导致 PTB 的分子机制和途径提供了新的见解。
Preterm birth (PTB) complicates more than 12% of all deliveries. Despite significant research, the aetiology of most cases of PTB remains elusive. Two major antecedents of PTB, intra-amniotic infection and decidual haemorrhage (abruption), can exhibit dissimilar demographic and genetic predispositions, despite sharing common molecular and cellular pathways. The use of high-throughput, high-dimensional technologies reveals substantial crosstalk between the coagulation and inflammation pathways. Tissue factor, thrombin and cytokines are key mediators of this crosstalk. Abruptions are associated with excess thrombin generated from decidual-cell-expressed tissue factor. Although thrombin is a primary mediator of the coagulation cascade, it can also promote inflammation-associated PTB by enhancing expression of matrix metalloproteinase and neutrophil-chemoattracting and -activating chemokines. Here, we provide novel insights into the molecular mechanisms and pathways leading to PTB in the setting of placental abruption.