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.

中文翻译：

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亚精胺通过调节 RIPK1 介导的细胞死亡和炎症来限制糖尿病


我们建立了血管内皮细胞中条件性 NAT1 缺陷诱导的进行性糖尿病小鼠模型。NAT1 缺陷促进了 RIPK1 的激活，这是由于一种由亚精胺和脱氧 hyupisin 合酶介导的翻译后修饰，称为乙酰 hypusination。我们的结果表明，抑制 RIPK1 可用于治疗 2 型糖尿病和血管炎症。