{"title":"CD38和线粒体钙离子单向传输器导致了与年龄相关的造血干细胞功能障碍。","authors":"Connor S R Jankowski, Thomas Weichhart","doi":"10.1097/IN9.0000000000000048","DOIUrl":null,"url":null,"abstract":"<p><p>Hematopoietic stem cells (HSCs) are the multipotent progenitors of all immune cells. During aging, their regenerative capacity decreases for reasons that are not well understood. Recently, Song et al investigated the roles of two metabolic proteins in age-related HSC dysfunction: CD38 (a membrane-bound NADase) and the mitochondrial calcium uniporter that transports calcium into the mitochondrial matrix. They found that the interplay between these proteins is deranged in aged HSCs, contributing to their diminished renewal capacity. These findings implicate compromised nicotinamide adenine dinucleotide metabolism as underlying HSC dysfunction in aging.</p>","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"6 4","pages":"e00048"},"PeriodicalIF":0.0000,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462411/pdf/","citationCount":"0","resultStr":"{\"title\":\"CD38 and the mitochondrial calcium uniporter contribute to age-related hematopoietic stem cell dysfunction.\",\"authors\":\"Connor S R Jankowski, Thomas Weichhart\",\"doi\":\"10.1097/IN9.0000000000000048\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Hematopoietic stem cells (HSCs) are the multipotent progenitors of all immune cells. During aging, their regenerative capacity decreases for reasons that are not well understood. Recently, Song et al investigated the roles of two metabolic proteins in age-related HSC dysfunction: CD38 (a membrane-bound NADase) and the mitochondrial calcium uniporter that transports calcium into the mitochondrial matrix. They found that the interplay between these proteins is deranged in aged HSCs, contributing to their diminished renewal capacity. These findings implicate compromised nicotinamide adenine dinucleotide metabolism as underlying HSC dysfunction in aging.</p>\",\"PeriodicalId\":73349,\"journal\":{\"name\":\"Immunometabolism (Cobham (Surrey, England))\",\"volume\":\"6 4\",\"pages\":\"e00048\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-10-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462411/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Immunometabolism (Cobham (Surrey, England))\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1097/IN9.0000000000000048\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunometabolism (Cobham (Surrey, England))","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/IN9.0000000000000048","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
造血干细胞是所有免疫细胞的多能祖细胞。在衰老过程中，造血干细胞的再生能力会下降，其原因尚不十分清楚。最近，Song 等人研究了两种代谢蛋白在与年龄相关的造血干细胞功能障碍中的作用：CD38（一种膜结合 NAD 酶）和线粒体钙单运器（将钙转运到线粒体基质中）。他们发现，在衰老的造血干细胞中，这些蛋白质之间的相互作用发生了改变，导致其更新能力减弱。这些发现表明，烟酰胺腺嘌呤二核苷酸代谢受到影响是衰老过程中造血干细胞功能障碍的根本原因。
CD38 and the mitochondrial calcium uniporter contribute to age-related hematopoietic stem cell dysfunction.
Hematopoietic stem cells (HSCs) are the multipotent progenitors of all immune cells. During aging, their regenerative capacity decreases for reasons that are not well understood. Recently, Song et al investigated the roles of two metabolic proteins in age-related HSC dysfunction: CD38 (a membrane-bound NADase) and the mitochondrial calcium uniporter that transports calcium into the mitochondrial matrix. They found that the interplay between these proteins is deranged in aged HSCs, contributing to their diminished renewal capacity. These findings implicate compromised nicotinamide adenine dinucleotide metabolism as underlying HSC dysfunction in aging.
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