biostudies-literatureWei XJilin Provincial Natural Science FoundationDepartment of Science and Technology of Jilin Province28032https://www.ebi.ac.uk/biostudies/studies/S-EPMC11564816biostudies-literatureUnknown14(1)Renal fibrosis is a common outcome of chronic kidney diseases and glycolysis drives the development of renal fibrosis in damaged kidneys. Ulinastatin (UTI) is a broad-spectrum protease inhibitor with anti-inflammatory and antioxidant properties with anti-fibrosis effects. In this study, we aimed to verify whether UTI could exert anti-renal fibrosis effects by inhibiting glycolysis and explored the potential mechanisms. Renal fibrosis was induced in mice via unilateral ureteral obstruction (UUO). Transforming growth factor-β1 stimulates human kidney proximal tubular epithelial cells to undergo fibrotic changes. Histopathological staining was used to observe the pathological changes in the kidneys. The levels of fibrosis biomarkers, glycolytic enzymes, and key signaling molecules were determScientific reportsUlinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis.PMC11564816YDZJ202301ZYTS012YDZJ202401170ZYTSYang LFan ZLong MWei XDu YHou YfalseUlinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis.Renal fibrosis is a common outcome of chronic kidney diseases and glycolysis drives the development of renal fibrosis in damaged kidneys. Ulinastatin (UTI) is a broad-spectrum protease inhibitor with anti-inflammatory and antioxidant properties with anti-fibrosis effects. In this study, we aimed to verify whether UTI could exert anti-renal fibrosis effects by inhibiting glycolysis and explored the potential mechanisms. Renal fibrosis was induced in mice via unilateral ureteral obstruction (UUO). Transforming growth factor-β1 stimulates human kidney proximal tubular epithelial cells to undergo fibrotic changes. Histopathological staining was used to observe the pathological changes in the kidneys. The levels of fibrosis biomarkers, glycolytic enzymes, and key signaling molecules were determ2024-01-01T00:00:00Z2024 Nov2026-06-02T03:36:55.611Z2025-04-05T18:41:20.3ZS-EPMC115648163954328510.1038/s41598-024-78092-0