Effect of FGF9 on human renal tubular epithelial cells in high glucose culture

Diabetic nephropathy is characterised by the accumulation of extracellular matrix in the glomerular tunica and tubular interstitium, which ultimately leads to excessive renal scarring and decreased excretory function. The main pathological changes of renal fibrosis are: glomerulosclerosis, tubulointerstitial fibrosis, infiltration of inflammatory mediators and activation of a-SMA-positive myofibroblasts. Among them, tubulointerstitial fibrosis is an important link in the development of end-stage renal disease (ESRD).Previous experiments verified that FGF9 expression was decreased in kidneys of STZ-induced diabetic mice and HK2 cells cultured with high glucose, while overexpression of FGF9 inhibited HK2 cell migration under high glucose. To investigate the role of FGF9 in tubulointerstitial fibrosis in diabetic nephropathy, we performed high-throughput sequencing of different subgroups of HK2 cells. Overall design: HK2 cells were divided into four groups: normal glucose group (NG), high glucose group (HG), high glucose + FGF9 overexpression group, and normal glucose + siRNA-FGF9 group.