{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yuan D"],"funding":["the Funding for Scientific Research and Innovation Team of the First Affiliated Hospital of Zhengzhou University","National Natural Science Foundation of China"],"pagination":["e02428"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12499423"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(37)"],"pubmed_abstract":["Acute lung injury (ALI) is a life-threatening condition with excessive immune activation and dysregulated inflammation. Dendritic cells (DCs) play a pivotal role in immune regulation; however, their exact contribution to ALI pathogenesis remains unclear. This study demonstrates that the upregulation of the glycolytic regulator 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2) by hypoxia-inducible factor-1α (HIF-1α) enhances glycolysis, drives DC maturation, and exacerbates inflammation, contributing to the pathogenesis of ALI. The findings reveal that HIF-1α directly binds to the PFKFB2 promoter and drives its transcription, leading to increased glycolysis, accelerated DC maturation, and amplified immune activation. In paraquat (PQ)-ALI and lipopolysaccharide (LPS)-ALI mouse "],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["PFKFB2-Driven Glycolysis Promotes Dendritic Cell Maturation and Exacerbates Acute Lung Injury."],"pmcid":["PMC12499423"],"funding_grant_id":["82172180;82302483;82472239;82402576;82372215","QNCXTD2023004"],"pubmed_authors":["Du Y","Zhu H","Zhang M","Pang X","Yang F","Cheng Y","Jiang P","Yuan D","Hou L","Jiang Y","Guo M","Li Y","Guo J","Zhang Y","Gao Y","Hao H","Yan H","Wu Y"],"additional_accession":[]},"is_claimable":false,"name":"PFKFB2-Driven Glycolysis Promotes Dendritic Cell Maturation and Exacerbates Acute Lung Injury.","description":"Acute lung injury (ALI) is a life-threatening condition with excessive immune activation and dysregulated inflammation. Dendritic cells (DCs) play a pivotal role in immune regulation; however, their exact contribution to ALI pathogenesis remains unclear. This study demonstrates that the upregulation of the glycolytic regulator 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2) by hypoxia-inducible factor-1α (HIF-1α) enhances glycolysis, drives DC maturation, and exacerbates inflammation, contributing to the pathogenesis of ALI. The findings reveal that HIF-1α directly binds to the PFKFB2 promoter and drives its transcription, leading to increased glycolysis, accelerated DC maturation, and amplified immune activation. In paraquat (PQ)-ALI and lipopolysaccharide (LPS)-ALI mouse ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-07-15T05:51:55.605Z","creation":"2026-06-30T03:16:14.779Z"},"accession":"S-EPMC12499423","cross_references":{"pubmed":["40736063"],"doi":["10.1002/advs.202502428"]}}