Key result
FTO gene deficiency attenuates renal tubulointerstitial fibrosis and alpha-SMA expression following ureteral obstruction in mice.
Why the study?
Does FTO deficiency reduce fibrogenic responses and renal fibrosis in a mouse model of obstructive nephropathy?
Does FTO deficiency reduce fibrogenic responses and renal fibrosis in a mouse model of obstructive nephropathy?
p-value: p=<0.05
FTO deficiency attenuates fibrogenic responses and extracellular matrix synthesis in a mouse model of obstructive nephropathy, suggesting a potential therapeutic target for renal fibrosis.
FTO may represent an antifibrotic target in obstructive nephropathy; hypothesis-generating in mice and requires human validation.
Genome-wide association studies have shown that variants in fat mass and obesity-associated (FTO) gene are robustly associated with body mass index and obesity. These FTO variants are also associated with end stage renal disease and all-cause mortality in chronic kidney diseases. However, the exact role of FTO in kidneys is currently unknown. Here we show that FTO expression is increased after ureteral obstruction and renal fibrosis. Deficiency of the FTO gene attenuates the fibrogenic responses induced by ureteral obstruction in the kidney. Renal tubular cells deficient of FTO produce less α-SMA after TGF-β stimulation. FTO is indispensable for the extracellular matrix synthesis after ureteral obstruction in kidneys. Indeed, global gene transcriptions amplitude is reduced in FTO deficient kidneys after ureteral obstruction. These data establish the importance of FTO in renal fibrosis, which may have potential therapeutic implications.
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Wang et al. (2016) studied Obstructive nephropathy and renal fibrosis. FTO gene deficiency vs. Wild-type mice was evaluated on Renal tubulointerstitial fibrosis and alpha-SMA expression (p=<0.05). FTO gene deficiency significantly attenuated renal tubulointerstitial fibrosis and decreased alpha-SMA protein expression following ureteral obstruction in mice.
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