探讨低雌激素状态诱发绝经后高血压的代谢组学机制

Yao Li, Hui Xin, Zhexun Lian, Wei Zhang
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引用次数: 0

摘要

背景:雌激素对女性的健康有重大影响,绝经后高血压是以血压波动为特征的常见问题。目前针对这种情况的控制策略效果有限,因此有必要进一步研究其潜在机制。虽然代谢组学已被应用于多种疾病的研究,但用于了解绝经后高血压的研究还很少:方法:使用卵巢切除大鼠模型模拟绝经后状况。分析雌激素水平、血压和主动脉组织代谢组学。动物模型分为 Sham 组、OVX 组和 OVX+E 组。利用放射免疫分析、超高效液相色谱-质谱(UHPLC-Q-TOF)和生物信息学技术对血清雌激素水平、血压测量和主动脉组织代谢组学进行了分析:结果:该研究成功确定了低雌激素水平与大鼠绝经后高血压之间的相关性。各实验组的血压参数和主动脉组织代谢物存在显著差异。具体而言,差异表达的代谢物,尤其是 L-α-氨基丁酸(L-AABA),显示出作为绝经后高血压生物标志物的潜力,可能通过巨噬细胞活化和血管重塑发挥保护功能。富集分析揭示了糖代谢途径的改变,如沃伯格效应和糖酵解,表明它们与绝经后高血压有关:这项研究深入揭示了与绝经后高血压相关的代谢变化,强调了 AABA 和糖代谢重编程在主动脉组织中的作用。研究结果表明,在绝经后高血压的发病机制中,低雌激素水平、巨噬细胞功能和血管重塑之间存在潜在联系。要验证这些发现并探讨其对绝经后妇女的临床意义,还需要进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exploration of the Metabolomic Mechanisms of Postmenopausal Hypertension Induced by Low Estrogen State
Background: Estrogen significantly impacts women's health, and postmenopausal hypertension is a common issue characterized by blood pressure fluctuations. Current control strategies for this condition are limited in efficacy, necessitating further research into the underlying mechanisms. Although metabolomics has been applied to study various diseases, its use in understanding postmenopausal hypertension is scarce. Methods: An ovariectomized rat model was used to simulate postmenopausal conditions. Estrogen levels, blood pressure, and aortic tissue metabolomics were analyzed. Animal models were divided into Sham, OVX, and OVX+E groups. Serum estrogen levels, blood pressure measurements, and aortic tissue metabolomics analyses were performed using radioimmunoassay, UHPLC-Q-TOF, and bioinformatics techniques. Results: The study successfully established a correlation between low estrogen levels and postmenopausal hypertension in rats. Notable differences in blood pressure parameters and aortic tissue metabolites were observed across the experimental groups. Specifically, metabolites that were differentially expressed, particularly L-alpha-aminobutyric acid (L-AABA), showed potential as a biomarker for postmenopausal hypertension, potentially exerting a protective function through macrophage activation and vascular remodeling. Enrichment analysis revealed alterations in sugar metabolism pathways, such as the Warburg effect and glycolysis, indicating their involvement in postmenopausal hypertension. Conclusion: This research provides insights into the metabolic changes associated with postmenopausal hypertension, highlighting the role of AABA and sugar metabolism reprogramming in aortic tissue. The findings suggest a potential link between low estrogen levels, macrophage function, and vascular remodeling in the pathogenesis of postmenopausal hypertension. Further investigations are needed to validate these findings and explore their clinical implications for postmenopausal women.
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