{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen Y"],"funding":["Life and Health Special Project of Hefei Science and Technology Bureau","2023 Research Project of the Institute of Xin'an Medicine and Modernization of Traditional Chinese Medicine, Institute of Health Sciences, Hefei Comprehensive National Science Center","2023 Research Project of the Institute of Xin'an Medicine and Modernization of Traditional Chinese Medicine, Institute of Health Sciences, Hefei Comprehensive National Science Center","Natural Science Foundation of Anhui Province","National Natural Science Foundation of China","Clinical Research Project of Anhui University of Chinese Medicine","Health Research Project of Anhui Provincial Health Commission"],"pagination":["121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12932785"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["83(1)"],"pubmed_abstract":["Glycolytic reprogramming is closely associated with chronic kidney disease (CKD) progression. However, the role and mechanism of phosphofructokinase muscle type (PFKM), a core rate-limiting enzyme in glycolysis, in renal fibrosis remain unclear. This study analyzed Gene Expression Omnibus (GEO) datasets of renal tissues from patients with CKD to construct a folic acid (FA)-induced mouse model of renal fibrosis. PFKM overexpression or knockdown was achieved specifically in renal tubular epithelial cells using an adeno-associated virus serotype 9 (AAV9) vector. Additionally, combined with a transforming growth factor-β1 (TGF-β1)-stimulated human kidney-2 (HK-2) cell model, the underlying mechanism was explored via histological staining, metabolic analysis, ribonucleic acid (RNA) sequencing ("],"journal":["Cellular and molecular life sciences : CMLS"],"pubmed_title":["The glycolytic enzyme PFKM promotes renal fibrosis by activating the NF-κB pathway via lactate-mediated H3K18 lactylation."],"pmcid":["PMC12932785"],"funding_grant_id":["2023CXMMTCM018","AHWJ2024BAc20084, AHWJ2024Aa30409","GJ2022SM03","2308085MH292, 2408085QH282","2024YFYLCZX28","82274307"],"pubmed_authors":["Zhang W","Dai R","Gao Y","Chen Y","Wang W","Cheng M","Zhang L","Sang Y","Wang Y","Wei L"],"additional_accession":[]},"is_claimable":false,"name":"The glycolytic enzyme PFKM promotes renal fibrosis by activating the NF-κB pathway via lactate-mediated H3K18 lactylation.","description":"Glycolytic reprogramming is closely associated with chronic kidney disease (CKD) progression. However, the role and mechanism of phosphofructokinase muscle type (PFKM), a core rate-limiting enzyme in glycolysis, in renal fibrosis remain unclear. This study analyzed Gene Expression Omnibus (GEO) datasets of renal tissues from patients with CKD to construct a folic acid (FA)-induced mouse model of renal fibrosis. PFKM overexpression or knockdown was achieved specifically in renal tubular epithelial cells using an adeno-associated virus serotype 9 (AAV9) vector. Additionally, combined with a transforming growth factor-β1 (TGF-β1)-stimulated human kidney-2 (HK-2) cell model, the underlying mechanism was explored via histological staining, metabolic analysis, ribonucleic acid (RNA) sequencing (","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-16T21:39:27.578Z","creation":"2026-07-10T03:15:12.869Z"},"accession":"S-EPMC12932785","cross_references":{"pubmed":["41711888"],"doi":["10.1007/s00018-026-06118-z"]}}