HNF3a targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury
Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3a expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3a in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3a promotes renal fibrosis, we transfected TKPTS cells with Hnf3a overexpression plasmids or control plasmids, and then performed transcriptome sequencing. Overall design: TKPTS cells were cultured in 6-well plates and transfected with pcDNA3.1-Hnf3a-Flag or pcDNA3.1-Flag. Twenty-four hours later, the cells were harvested for transcriptome sequencing.