Authors
Chi Zhang, Rui Ge, Min Liu, Jianhuai Huang, Jingyu Cai, Tao Sun, Sheng Ge, Qiuchen Li, Yuanyuan Zhang
Published in
Journal of cellular and molecular medicine. Volume 30. Issue 20. Pages e71369.
Abstract
Renal fibrosis, a defining feature of chronic kidney disease, involves a metabolic shift toward aerobic glycolysis and is frequently accompanied by ferroptosis, a form of iron-dependent cell death. This study investigated the therapeutic potential of adipose mesenchymal stem cell-derived exosomes (AMSC-exo) in renal fibrosis. Using a unilateral ureteral obstruction (UUO) mouse model and hypoxia-treated HK-2 cells, we assessed fibrosis, glycolysis, mitochondrial morphology, and ferroptosis. miRNA sequencing, dual-luciferase reporter assays, and transcriptome sequencing were performed to identify key exosomal miRNAs and downstream pathways. AMSC-exo significantly attenuated UUO-induced fibrosis and suppressed glycolysis and ferroptosis in tubular epithelial cells. miR-26a-5p was highly enriched in AMSC-exo and downregulated 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (Pfkfb3), a key regulator of glycolysis and ferroptosis. Knockdown of miR-26a-5p markedly weakened the renoprotective effects of AMSC-exo, whereas Pfkfb3 inhibition reversed the effects induced by miR-26a-5p deficiency. These findings indicate that AMSC-exo alleviate renal fibrosis by delivering miR-26a-5p to suppress Pfkfb3, thereby inhibiting glycolytic reprogramming and ferroptosis, and suggest the miR-26a-5p/Pfkfb3 axis as a potential therapeutic target for renal fibrosis.
PMID:
42885940
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.
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