In the present study, Trib1 depletion depressed cell viability by inhibiting proliferation of renal tubular epithelial cells and inducing cell apoptosis in vitro, caused the same symptoms of renal dysfunction as I/R administration in vivo, and Trib1 depletion or I/R stimulation-induced renal dysfunction was restored by the self-repair systems in mice. The gene discussed is TRIB1; the disease is Abnormal renal physiology.