{"title":"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","authors":"","doi":"10.1038/s41556-024-01542-4","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"37 1","pages":""},"PeriodicalIF":17.3000,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Spermidine limits diabetes by modulating RIPK1-mediated cell death and inflammation\",\"authors\":\"\",\"doi\":\"10.1038/s41556-024-01542-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":18977,\"journal\":{\"name\":\"Nature Cell Biology\",\"volume\":\"37 1\",\"pages\":\"\"},\"PeriodicalIF\":17.3000,\"publicationDate\":\"2024-11-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Cell Biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1038/s41556-024-01542-4\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Cell Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s41556-024-01542-4","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
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.
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
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