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High‐mobility group box 1 is a driver of inflammation throughout pregnancy
American Journal of Reproductive Immunology ( IF 3.6 ) Pub Date : 2020-08-27 , DOI: 10.1111/aji.13328
Chelsea A Saito Reis 1 , Justin G Padron 2 , Nainoa D Norman Ing 1 , Claire E Kendal-Wright 1, 2, 3
Affiliation  

A proinflammatory response driven by high‐mobility group box 1 (HMGB1) is important for the success of both the early stages of pregnancy and parturition initiation. However, the tight regulation of HMGB1 within these two stages is critical, as increased HMGB1 can manifest into pregnancy‐related pathologies. Although during the early stages of pregnancy HMGB1 is critical for the development and implantation of the embryo, and uterine decidualization, high levels within the uterine cavity have been linked to pregnancy failure. In addition, chronic inflammation, resultant from increased HMGB1 within the maternal circulation and gestational tissues, also increases the risk for preterm labor, preterm birth, or infant mortality. Due to the link between HMGB1 and several pregnancy pathologies, the possibility of leveraging HMGB1 as a biomarker has been assessed. However, data are limited that demonstrate how known HMGB1 inhibitors could reduce inflammation within pregnancy. Thus, further research is warranted to improve our understanding of the potential of HMGB1 as a therapeutic target to reduce inflammation within pregnancy. This review aims to describe what is understood about the role of HMGB1 that drives inflammation throughout pregnancy and highlight its potential as a biomarker and therapeutic target within this context.

中文翻译:

高机动性群箱 1 是整个孕期炎症的驱动因素

由高迁移率族框 1 (HMGB1) 驱动的促炎反应对于妊娠早期和分娩开始的成功都很重要。然而,在这两个阶段内对 HMGB1 的严格调节至关重要,因为 HMGB1 的增加可以表现为与妊娠相关的病理。尽管在妊娠早期 HMGB1 对胚胎的发育和植入以及子宫蜕膜化至关重要,但宫腔内的高水平与妊娠失败有关。此外,由母体循环和妊娠组织中 HMGB1 增加引起的慢性炎症也会增加早产、早产或婴儿死亡的风险。由于 HMGB1 与几种妊娠病理之间的联系,已经评估了利用 HMGB1 作为生物标志物的可能性。然而,证明已知 HMGB1 抑制剂如何减少妊娠期炎症的数据有限。因此,需要进一步研究以提高我们对 HMGB1 作为减少妊娠期炎症的治疗靶点的潜力的理解。本综述旨在描述人们对 HMGB1 在整个妊娠期间引发炎症的作用的理解,并强调其在此背景下作为生物标志物和治疗靶点的潜力。
更新日期:2020-08-27
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