Potential role of uric acid to activate NLRP3 inflammasome triggering endothelial dysfunction in preeclampsia

Priscila Rezeck Nunes , Mariana Romao-Veiga , Maria Terezinha Serrao Peracoli , Jose Carlos Peracoli , Valeria Cristina Sandrim
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引用次数: 2

Abstract

Preeclampsia (PE) is a pregnancy-related disorder associated with increasing maternal death rates and affecting 2–8% of pregnant women worldwide. Arterial hypertension and proteinuria, followed by other maternal dysfunctions are classic clinical parameters to identify this disease. Furthermore, hyperuricemia is strictly related to PE, and high plasmatic levels of uric acid have been associated with disease severity. The inflammation in the endothelium caused by danger signals, such as uric acid crystals, is persistent and stimulates the release of inflammatory cytokines, and activates the NLRP3 inflammasome. The mechanisms underlying endothelial dysfunction induced by the metabolism of uric acid, and consequently increased levels of inflammation and oxidative stress in women with PE could be ameliorated with interventions related to inhibition of the NLRP3 activation MSU-mediated and may improve the prognostics of this disease.

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尿酸激活NLRP3炎性体引发子痫前期内皮功能障碍的潜在作用
子痫前期(PE)是一种妊娠相关疾病,与孕产妇死亡率上升有关,影响全世界2-8%的孕妇。动脉高血压和蛋白尿,其次是其他产妇功能障碍是诊断该病的典型临床参数。此外,高尿酸血症与PE密切相关,高血浆尿酸水平与疾病严重程度相关。尿酸结晶等危险信号引起的内皮炎症是持续性的,刺激炎症因子的释放,激活NLRP3炎性小体。尿酸代谢诱导的内皮功能障碍的机制,以及由此导致的PE女性炎症和氧化应激水平的升高,可以通过抑制msu介导的NLRP3激活的干预措施得到改善,并可能改善该疾病的预后。
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