精胺通过调节 RIPK1 介导的细胞死亡和炎症限制糖尿病的发生

IF 17.3 1区生物学 Q1 CELL BIOLOGY

Nature Cell Biology Pub Date : 2024-11-07 DOI:10.1038/s41556-024-01542-4

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引用次数: 0

摘要

我们在血管内皮细胞中建立了一个由条件性 NAT1 缺乏诱导的进行性糖尿病小鼠模型。NAT1 缺乏会促进 RIPK1 的活化，这是一种由亚精胺和脱氧羽扇豆素合成酶介导的翻译后修饰（称为乙酰化）所致。我们的研究结果表明，抑制 RIPK1 可用于治疗 2 型糖尿病和血管炎症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Spermidine limits diabetes by modulating RIPK1-mediated cell death and inflammation

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Spermidine limits diabetes by modulating RIPK1-mediated cell death and inflammation

We establish a mouse model of progressive diabetes induced by conditional NAT1 deficiency in vascular endothelial cells. NAT1 deficiency promotes the activation of RIPK1 owing to a type of post-translational modification mediated by spermidine and deoxyhyupisin synthase termed acetyl-hypusination. Our results suggest that inhibition of RIPK1 could be used to treat type 2 diabetes and vascular inflammation.

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来源期刊

Nature Cell Biology 生物-细胞生物学

CiteScore

28.40

自引率

0.90%

发文量

219

审稿时长

3 months

期刊介绍： Nature Cell Biology, a prestigious journal, upholds a commitment to publishing papers of the highest quality across all areas of cell biology, with a particular focus on elucidating mechanisms underlying fundamental cell biological processes. The journal's broad scope encompasses various areas of interest, including but not limited to: -Autophagy -Cancer biology -Cell adhesion and migration -Cell cycle and growth -Cell death -Chromatin and epigenetics -Cytoskeletal dynamics -Developmental biology -DNA replication and repair -Mechanisms of human disease -Mechanobiology -Membrane traffic and dynamics -Metabolism -Nuclear organization and dynamics -Organelle biology -Proteolysis and quality control -RNA biology -Signal transduction -Stem cell biology