C/EBP homologous protein (CHOP) deficiency ameliorates renal fibrosis in unilateral ureteral obstructive kidney disease

• DOI: 10.18632/oncotarget.7870
• Publication Date: 2016-03-03T07:20:15Z
• Authors: Shing-Hwa Liu; Cheng-Tien Wu; Kuo-How Huang; Ching-Chia Wang; Siao-Syun Guan; Li-Ping Chen; Chih-Kang Chiang
• Keywords: Mice, Knockout; Mice; 0303 health sciences; 03 medical and health sciences; Animals; Renal Insufficiency, Chronic; Fibrosis; Transcription Factor CHOP; Research Paper; Ureteral Obstruction; 3. Good health

Renal tubulointerstitial fibrosis is an important pathogenic feature in chronic kidney disease and end-stage renal disease, regardless of the initiating insults. A recent study has shown that CCAAT/enhancer binding protein (C/EBP) homologous (CHOP) involved acute ischemia/reperfusion-related injury through oxidative stress induction. However, influence CHOP on disease-correlated remains unclear. Here, we investigated role unilateral ureteral obstruction (UUO)-induced experimental tubulointerstital fibrosis. The knockout wild type mice with or without UUO were used. results showed increased expressions markers collagen I, fibronectin, α-smooth muscle actin, plasminogen activator inhibitor-1 kidneys UUO-treated dramatically attenuated mice. deficiency could also ameliorate lipid peroxidation endogenous antioxidant enzymes depletion, tubular apoptosis, inflammatory cells infiltration kidneys. These suggest not only attenuates apoptotic death fibrosis, but reduces local inflammation, leading to diminish UUO-induced Our findings support may be signaling molecule progression disease.