{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gu J"],"funding":["Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences","National Key Research and Development Program of China Stem Cell and Translational Research","National Natural Science Foundation of China","Natural Science Foundation of Guangdong Province","Innovation and Technology Commission","Youth Innovation Promotion Association of the Chinese Academy of Sciences"],"pagination":["196-210"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10874853"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(2)"],"pubmed_abstract":["Emergency myelopoiesis (EM) is essential in immune defense against pathogens for rapid replenishing of mature myeloid cells. During the EM process, a rapid cell-cycle switch from the quiescent hematopoietic stem cells (HSCs) to highly proliferative myeloid progenitors (MPs) is critical. How the rapid proliferation of MPs during EM is regulated remains poorly understood. Here, we reveal that ATG7, a critical autophagy factor, is essential for the rapid proliferation of MPs during human myelopoiesis. Peripheral blood (PB)-mobilized hematopoietic stem/progenitor cells (HSPCs) with ATG7 knockdown or HSPCs derived from ATG7<sup>-/-</sup> human embryonic stem cells (hESCs) exhibit severe defect in proliferation during fate transition from HSPCs to MPs. Mechanistically, we show that ATG7 deficien"],"journal":["Stem cell reports"],"pubmed_title":["Autophagy is essential for human myelopoiesis."],"pmcid":["PMC10874853"],"funding_grant_id":["2020A1515010139","2022YFA1105000","31971374","32171451","32270624"],"pubmed_authors":["Chen Q","Mai Y","Zhu Y","Guo X","Li F","Hu X","Zhou T","Wang J","Wang M","Pan G","Shan Y","Huang Y","Kang B","Gao M","Zhang Z","Zhang Y","Wang S","Cui Y","Lin H","Gu J","Xing Q","Peng J","Long B"],"additional_accession":[]},"is_claimable":false,"name":"Autophagy is essential for human myelopoiesis.","description":"Emergency myelopoiesis (EM) is essential in immune defense against pathogens for rapid replenishing of mature myeloid cells. During the EM process, a rapid cell-cycle switch from the quiescent hematopoietic stem cells (HSCs) to highly proliferative myeloid progenitors (MPs) is critical. How the rapid proliferation of MPs during EM is regulated remains poorly understood. Here, we reveal that ATG7, a critical autophagy factor, is essential for the rapid proliferation of MPs during human myelopoiesis. Peripheral blood (PB)-mobilized hematopoietic stem/progenitor cells (HSPCs) with ATG7 knockdown or HSPCs derived from ATG7<sup>-/-</sup> human embryonic stem cells (hESCs) exhibit severe defect in proliferation during fate transition from HSPCs to MPs. Mechanistically, we show that ATG7 deficien","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2026-07-14T16:26:29.315Z","creation":"2025-04-19T07:34:26.934Z"},"accession":"S-EPMC10874853","cross_references":{"pubmed":["38215759"],"doi":["10.1016/j.stemcr.2023.12.005"]}}