The glycolytic enzyme PFKM promotes renal fibrosis by activating the NF-κB pathway via lactate-mediated H3K18 lactylation.

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 (

SUBMITTER: Chen Y 

PROVIDER: S-EPMC12932785 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature