{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Z"],"funding":["NCI NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health"],"pagination":["396"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9051098"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(1)"],"pubmed_abstract":["Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabo"],"journal":["Communications biology"],"pubmed_title":["Loss of SIRT1 inhibits hematopoietic stem cell aging and age-dependent mixed phenotype acute leukemia."],"pmcid":["PMC9051098"],"funding_grant_id":["P30CA33572","UH3 CA213385","CA143421","R21 CA263223","R01 CA143421","P30 CA033572","CA213385","UH2 CA213385"],"pubmed_authors":["Wang C","Wang J","Brown C","Liu Z","Yang Y","Forman S","Chen W","Yuan YC","Guo C","Wang X","James You M","Zhang C","Warden CD","Ermel R","Wang Z","Vonderfecht SL","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"Loss of SIRT1 inhibits hematopoietic stem cell aging and age-dependent mixed phenotype acute leukemia.","description":"Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabo","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-03-18T13:41:44.71Z","creation":"2025-04-05T13:23:16.986Z"},"accession":"S-EPMC9051098","cross_references":{"pubmed":["35484199"],"doi":["10.1038/s42003-022-03340-w"]}}