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Elevated S100A9 in preeclampsia induces soluble endoglin and IL-1β secretion and hypertension via the NLRP3 inflammasome.
Journal of Hypertension ( IF 3.3 ) Pub Date : 2021-08-18 , DOI: 10.1097/hjh.0000000000002981
Ayae Ozeki 1 , Yuka Oogaki 1 , Yuka Henmi 1 , Tadayoshi Karasawa 2 , Masafumi Takahashi 2 , Hironori Takahashi 3 , Akihide Ohkuchi 3 , Koumei Shirasuna 1
Affiliation  

Maternal systemic and placental inflammatory responses participate in the pathogenesis of hypertensive disorders of pregnancy including preeclampsia, a pregnancy-specific syndrome, although the role of inflammation remains unclear. The NLRP3 inflammasome has been implicated in the control of sterile inflammation involved in preeclampsia. In the present study, we hypothesized that S100A9, as major alarmin, are associated with the pathogenesis of preeclampsia and induction of a preeclampsia-like phenotype in pregnant mice.

中文翻译:

先兆子痫中升高的 S100A9 通过 NLRP3 炎性体诱导可溶性内皮糖蛋白和 IL-1β 分泌和高血压。

母体全身和胎盘炎症反应参与妊娠高血压疾病的发病机制,包括先兆子痫,一种妊娠特异性综合征,尽管炎症的作用仍不清楚。NLRP3 炎性体与控制先兆子痫相关的无菌炎症有关。在本研究中,我们假设 S100A9 作为主要的警报素,与妊娠小鼠先兆子痫的发病机制和诱导子痫前期样表型有关。
更新日期:2021-08-18
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