尿苷磷酸化酶1在急性肺损伤中与糖酵解相关的生物标志物

IF 4.5 2区 医学 Q2 CELL BIOLOGY
Congkuan Song, Qingqing Li, Jinjin Zhang, Weidong Hu
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引用次数: 0

摘要

急性肺损伤(acute lung injury, ALI)的具体发病机制复杂且尚不清楚,临床治疗方法也相对有限。探讨其发病机制和有效的分子靶点具有重要的临床意义。在这里,我们通过系统的生物信息学方法确定了与尿苷代谢相关的ALI生物标志物(UPP1)。在小鼠ALI模型中也证实其与糖酵解途径相关。此外,基于CMAP数据库的药物敏感性分析确定了三种可能用于治疗ALI的upp1相关药物(CAY10585、XL147和IOX2)。分子对接和分子动力学模拟进一步证实了UPP1与三种药物结合的稳定性。总之,本研究证实与糖酵解相关的尿苷代谢基因UPP1是ALI的关键生物标志物,为CAY10585、XL147和IOX2在ALI中的潜在应用提供了有价值的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Uridine Phosphorylase 1 as a Biomarker Associated with Glycolysis in Acute Lung Injury.

The specific pathogenesis of acute lung injury (ALI) is complex and not yet clear, and the clinical treatment methods are relatively limited. It is of great clinical significance to explore its pathogenesis and effective molecular targets. Here, we identified an ALI biomarker (UPP1) associated with uridine metabolism by a systematic bioinformatics approach. It was also confirmed to be associated with the glycolytic pathway in the mouse ALI model. In addition, drug sensitivity analysis based on the CMAP database identified three UPP1-associated drugs (CAY10585, XL147 and IOX2) that may be useful in the treatment of ALI. Molecular docking and molecular dynamics simulations further confirmed the stability of the binding between UPP1 and the three drugs. In conclusion, this study confirms that the uridine metabolism gene UPP1 associated with glycolysis is a key biomarker of ALI and provides valuable insights into the potential application of CAY10585, XL147 and IOX2 in ALI.

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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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