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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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The levels of fibroblast growth factor 23 (FGF23) increase rapidly after acute kidney injury (AKI); however, its precise role in AKI is still unclear.
Circulating levels of FGF23 in 96 adults admitted to the intensive care unit (ICU) was analyzed. In vivo and in vitro folic acid (FA)-induced acute kidney injury (AKI) models were employed to investigate the role of FGF23, through inhibition using FGF receptor (FGFR) inhibitors or enhancement via recombinant human FGF23 (rhFGF23) protein.
Serum intact FGF23 (iFGF23) and C-terminal FGF23 (cFGF23) were significantly increased in AKI patients. In FA-AKI mice, serum creatinine and blood urea nitrogen levels were significantly elevated, and histological analysis showed tubular and interstitial injury. FA stimulation of HK-2 cells led to decreased cell viability which indacted significant injury.
Serum FGF23 and renal FGF23 protein levels were significantly increased in FA-AKI mice (Fig. 1 A and B). In vitro, FGF23 levels were also elevated progressively with higher FA concentrations and extended stimulation periods (Fig. 1 C and D). Transmission electron microscopy (TEM) strongly suggests the occurrence of pyroptosis in FA-AKI characterized by balloon-like bubbles on the cell membrane and membrane rupture (Fig. 1 E). The expression levels of GSDME-NT and cleaved-caspase 3 increased in both in vivo and in vitro FA-AKI models (Fig. 1 F, G, and H). Immunofluorescence staining demonstrated the upregulation of GSDME in both the in vivo and in vitro FA-AKI groups (Fig. 1 I and J). Blocking caspase-3 activation with Z-DEVD-FMK prevented GSDME cleavage, ultimately halting pyroptosis.
Western blot analysis indicated that the levels of LC3B-II were significantly elevated both in vivo and in vitro FA-AKI models (Fig. 2 A, B and C). Immunofluorescence images exhibited the upregulation of LC3B-II in the renal tubular epithelial cells of the AKI group as well as in renal tissue from FA-AKI mice (Fig. 2D and E). Furthermore, autophagy in FA-AKI was confirmed in vitro through TEM observations of autophagosomes and autolysosomes (Fig. 2F).
FGFR pan-inhibitor PD173074 led to reduced cell viability and increased lactic dehydrogenase (LDH) levels compared to the FA group. Additionally, the levels of LC3B-II were significantly reduced, while the levels of cleaved-caspase 3 and GSDME-NT were significantly elevated. The FGFR4 specific inhibitor BLU9931 showed similar results. In contrast, administration of rhFGF23 resulted in opposite results (Fig. 2G, H, and I). In summary, FGF23 enhances autophagy and subsequently inhibits caspase-3/GSDME-mediated pyroptosis in FA-AKI.
Our study elucidated the protective role of FGF23 in AKI and clarified its underlying mechanism by targeting GSDME-mediated pyroptosis through autophagy.
