{"title":"用NAD+给老化的car充电以促进免疫治疗。","authors":"Gaofeng Fan, Yuetong Wang, Ruoning Wang","doi":"10.1016/j.trecan.2025.06.009","DOIUrl":null,"url":null,"abstract":"<p><p>Impaired cellular metabolism contributes to the age-related decline in T cell function, undermining the response to immunotherapy in older patients with cancer. In a recent study, Hope et al. report that a reduction in intracellular NAD<sup>+</sup> levels compromises metabolic fitness and drives immunosenescence. Notably, restoring NAD<sup>+</sup> levels can reverse age-related chimeric antigen receptor (CAR)-T deterioration, suggesting a promising 'metabolic immunotherapy' that widely benefits older patients with cancer.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":17.5000,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12210223/pdf/","citationCount":"0","resultStr":"{\"title\":\"Recharging aged-CAR with NAD<sup>+</sup> to boost immunotherapy.\",\"authors\":\"Gaofeng Fan, Yuetong Wang, Ruoning Wang\",\"doi\":\"10.1016/j.trecan.2025.06.009\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Impaired cellular metabolism contributes to the age-related decline in T cell function, undermining the response to immunotherapy in older patients with cancer. In a recent study, Hope et al. report that a reduction in intracellular NAD<sup>+</sup> levels compromises metabolic fitness and drives immunosenescence. Notably, restoring NAD<sup>+</sup> levels can reverse age-related chimeric antigen receptor (CAR)-T deterioration, suggesting a promising 'metabolic immunotherapy' that widely benefits older patients with cancer.</p>\",\"PeriodicalId\":23336,\"journal\":{\"name\":\"Trends in cancer\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":17.5000,\"publicationDate\":\"2025-06-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12210223/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Trends in cancer\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.trecan.2025.06.009\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Trends in cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.trecan.2025.06.009","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
Recharging aged-CAR with NAD+ to boost immunotherapy.
Impaired cellular metabolism contributes to the age-related decline in T cell function, undermining the response to immunotherapy in older patients with cancer. In a recent study, Hope et al. report that a reduction in intracellular NAD+ levels compromises metabolic fitness and drives immunosenescence. Notably, restoring NAD+ levels can reverse age-related chimeric antigen receptor (CAR)-T deterioration, suggesting a promising 'metabolic immunotherapy' that widely benefits older patients with cancer.
期刊介绍:
Trends in Cancer, a part of the Trends review journals, delivers concise and engaging expert commentary on key research topics and cutting-edge advances in cancer discovery and medicine.
Trends in Cancer serves as a unique platform for multidisciplinary information, fostering discussion and education for scientists, clinicians, policy makers, and patients & advocates.Covering various aspects, it presents opportunities, challenges, and impacts of basic, translational, and clinical findings, industry R&D, technology, innovation, ethics, and cancer policy and funding in an authoritative yet reader-friendly format.