{"title":"克隆优势:VEXAS综合征的突变利用炎症","authors":"Samuel J. Magaziner, David B. Beck","doi":"10.1038/s41584-025-01270-5","DOIUrl":null,"url":null,"abstract":"VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is caused by somatic mutations in UBA1 arising in hematopoietic stem cells, resulting in systemic autoinflammation and clonal outgrowth of these mutant cells. New research provides insights into the paradoxical mechanism behind this clonal hematopoietic dominance.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"21 9","pages":"511-512"},"PeriodicalIF":32.7000,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Clonal dominance: mutations in VEXAS syndrome take advantage of inflammation\",\"authors\":\"Samuel J. Magaziner, David B. Beck\",\"doi\":\"10.1038/s41584-025-01270-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is caused by somatic mutations in UBA1 arising in hematopoietic stem cells, resulting in systemic autoinflammation and clonal outgrowth of these mutant cells. New research provides insights into the paradoxical mechanism behind this clonal hematopoietic dominance.\",\"PeriodicalId\":18810,\"journal\":{\"name\":\"Nature Reviews Rheumatology\",\"volume\":\"21 9\",\"pages\":\"511-512\"},\"PeriodicalIF\":32.7000,\"publicationDate\":\"2025-06-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Reviews Rheumatology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.nature.com/articles/s41584-025-01270-5\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"RHEUMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Reviews Rheumatology","FirstCategoryId":"3","ListUrlMain":"https://www.nature.com/articles/s41584-025-01270-5","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
Clonal dominance: mutations in VEXAS syndrome take advantage of inflammation
VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is caused by somatic mutations in UBA1 arising in hematopoietic stem cells, resulting in systemic autoinflammation and clonal outgrowth of these mutant cells. New research provides insights into the paradoxical mechanism behind this clonal hematopoietic dominance.
期刊介绍:
Nature Reviews Rheumatology is part of the Nature Reviews portfolio of journals. The journal scope covers the entire spectrum of rheumatology research. We ensure that our articles are accessible to the widest possible audience.