{"title":"炎症和造血功能紊乱驱动小鼠VEXAS综合征模型的克隆优势","authors":"","doi":"10.1038/s41591-025-03670-2","DOIUrl":null,"url":null,"abstract":"We show that hematopoiesis in a mouse model of VEXAS syndrome is subverted by inflammation-resilient, senescent-like mutant HSPCs, which have dysfunctional differentiation and undermine hematopoiesis through their proinflammatory progeny. This disease mechanism explains clonal dominance and bone marrow failure (BMF) in patients with VEXAS syndrome and could have translational implications.","PeriodicalId":19037,"journal":{"name":"Nature Medicine","volume":"89 1","pages":""},"PeriodicalIF":58.7000,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Inflammation and disrupted hematopoiesis drive clonal dominance in a mouse model of VEXAS syndrome\",\"authors\":\"\",\"doi\":\"10.1038/s41591-025-03670-2\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We show that hematopoiesis in a mouse model of VEXAS syndrome is subverted by inflammation-resilient, senescent-like mutant HSPCs, which have dysfunctional differentiation and undermine hematopoiesis through their proinflammatory progeny. This disease mechanism explains clonal dominance and bone marrow failure (BMF) in patients with VEXAS syndrome and could have translational implications.\",\"PeriodicalId\":19037,\"journal\":{\"name\":\"Nature Medicine\",\"volume\":\"89 1\",\"pages\":\"\"},\"PeriodicalIF\":58.7000,\"publicationDate\":\"2025-04-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41591-025-03670-2\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41591-025-03670-2","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Inflammation and disrupted hematopoiesis drive clonal dominance in a mouse model of VEXAS syndrome
We show that hematopoiesis in a mouse model of VEXAS syndrome is subverted by inflammation-resilient, senescent-like mutant HSPCs, which have dysfunctional differentiation and undermine hematopoiesis through their proinflammatory progeny. This disease mechanism explains clonal dominance and bone marrow failure (BMF) in patients with VEXAS syndrome and could have translational implications.
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