胎盘甲基醇在妊娠前:血管和生物标志物影响
Philippe Vangrieken1, Salwan Al-Nasiry2, Alex H V Remels3
1School for Cardiovascular Diseases, Department of Internal Medicine (P.V., S.N., J.L.J.M.S., C.G.S.), Maastricht University Medical Center+, the Netherlands.
Hypertension (Dallas, Tex. : 1979)
|May 16, 2024
概括
在孕前症中,胎盘甲基醇 (MGO) 的增加有助于血管功能障碍. 早期检测可能使用等离子体生物标志物,如Nε-(carboxymethyl) lysine (CML) 和MG-H1.1可能是可能的.
科学领域:
- 产科和妇科 产科和妇科
- 血管生物学 血管生物学
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 孕前是一个怀孕并发症,其特点是母亲的血管功能障碍.
- 缺氧和增加的胎盘糖解都与孕前的发病因子有关.
- 甲基醇 (MGO) 是一种反应性二碳化合物,有可能将胎盘功能障碍与血管问题联系起来.
研究的目的:
- 为了研究胎盘甲基酸盐 (MGO) 在产前相关的血管功能障碍中的作用.
- 为了确定缺氧是否会增加胎盘组织中的MGO水平.
- 探索可能的孕前的早期生物标志物.
主要方法:
- 量化MGO和先进的糖化终产物 (CML,CEL,MG-H) 在产卵前和无并发症怀孕的胎盘中.
- 评估了glyoxalase-1 (GLO1) 活性,这是排毒MGO的酶.
- 暴露的胎盘组织和 trofhoblast 细胞低氧.
- 评估了MGO对血管功能的影响,使用肌肉图.
- 经过测试的MGO清除和抗氧化疗法 (quercetin,MitoQ).
主要成果:
- 结核前的胎盘显示MGO,CML,CEL和MG-H水平升高.
- 在孕前和缺氧暴露的胎盘中,GLO1活性降低了.
- 低氧增加了胎盘中的MGO,这种效应被氨酸逆转.
- 孕妇的血CML和MG-H1在怀孕早期增加.
- MGO损害了内皮屏障功能和增加了血管反应能力,MitoQ减轻了这些影响.
结论:
- 胎盘MGO积聚在妊娠前和缺氧,导致血管功能障碍.
- 减少GLO1活动在MGO积累中起作用.
- 血CML和MG-H1显示为早期孕前的生物标志物具有前途.
- 由MGO诱导的血管功能障碍可能是治疗点.
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